Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chloramines, compounds made up of chlorine and ammonia, when present in tap water used for dialysis cause methemoglobinemia and hemolysis. Ascorbic acid addition has been reported to effectively neutralize chloramines in vitro and in patients dialyzed with the single batch dialysis delivery system. We extended these observations to patients dialyzed with the proportioning dialysis delivery system where exposure time of ascorbic acid to chloramines is shorter. This may be important since we found that the half time of the reaction between ascorbic acid and chloramines is 4 minutes. Red cell oxidant sensitivity in 15 patients was assessed by incubating red cells with ascorbate-cyanide and measuring methemoglobin which averaged 2.17 +/- 0.42 g/100 ml (SEM) before dialysis and 2.87 +/- 0.52 g/100 ml after dialysis (NS). Reduced glutathione (GSH) levels were also measured as an index of red cell oxidant damage. GSH decreased from a mean of 7.40 +/- 0.59 micromoles/g Hb before dialysis to 6.98 +/- 0.52 micronmoles/g Hb after dialysis (P less than 0.01). In 2 patients there was no change in 51Cr red cell survival when dialyzed on either the proportioning system or other chloramine free systems. We conclude that addition of ascorbic acid to neutralize chloramines in tap water is also effective when using the proportioning dialysis delivery system.
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PMID:Prevention of chloramine-induced hemolysis in dialyzed patients. 69 6

In patients with chronic renal failure (CRF) (CCr less than 20 ml/min), we have previously demonstrated greater rates of Na excretion (ex) when Na intake was nearly all NaHCO3 as compared to NaCl (both 200 mEq Na daily). Chloride (Cl) wasting on NaHCO3 (with severe Cl restriction) occurred, however, and may in part explain the results. To avoid Cl restriction in 6 patients with CRF (CCr 10-15 ml/min) on an estimated 10 mEq Na and Cl diet, electrolyte ex was compared on NaCl supplements of 200 mEq/day versus a daily mixture of NaHCO3 (100mEq) and NaCl (100 mEq). Periods on NaCl and the mixture lasted 4 days (order randomized) separated by re-equilibration to baseline weight (wt). Mean +/- SEM ex of Na, Cl, HCO3 mEq/day and CCr and deltawt (lbs) are compared below for the 4th day of NaCl vs NaHCO3 intake. (see article). Also there were no significant differences in K excretion, blood pressure, or plasma renin activities. Mean serum HCO3 increased from 21.2 to 25.8 mEq/l (day 1 vs 5, P less than 0.01) reflecting the net positive HCO3 balance on the mixture indicated above. Thus increments of Na intake above a fixed NaCl intake were excreted similarly whether given as NaCl or NaHCO3. Greater Na ex on NaHCO3 may depend on severe Cl restriction and/or higher serum HCO3 levels. If dietary NaCl intakes are near maximum tolerance, NaHCO3 supplementation should be accompanied by reductions in NaCl intake to maintain Na balance,
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PMID:NaHCO3 and NaCl tolerance in chronic renal failure II. 83 32

Recombinant human insulin-like growth factor I (rhIGF-I) was administered subcutaneously to 6 normal subjects and 2 patients with GH deficiency at a dose of 0.1 mg/kg for 7 consecutive days after breakfast. In normal subjects, plasma IGF-I levels increased from 217 +/- 22 ng/ml (Mean +/- SEM) to maximal levels of 581 +/- 6 ng/ml 4 h after the first administration of IGF-I. The blood glucose levels were statistically depressed 4 h after injection at 69 +/- 2 mg/dl. Similar plasma IGF-I and blood glucose profiles were observed after the seventh administration of IGF-I. The free form of IGF-I in plasma was 2.3 +/- 0.3 ng/ml in normal subjects and increased to maximal levels of 43.5 +/- 5.1 ng/ml 2 h after the first IGF-I administration. A similar pattern for the free form of IGF-I was observed after the seventh administration; however, the values obtained at 0, 1 and 2 h were greater after the seventh administration. In patients with G-deficiency, the plasma IGF-I and blood glucose profiles were similar to those observed in normal subjects, although the total IGF-I levels were low in these patients at all sampling points during the study. Slight decreases in serum insulin, uric acid, and creatinine were observed after the seventh administration of IGF-I. There were no changes in the excretion of urea nitrogen, creatine, creatinine, sodium, potassium, chlorine, calcium or C-peptide in the urine during the 7 days of IGF-I administration.
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PMID:Repeated sc administration of recombinant human insulin-like growth factor I (IGF-I) to human subjects for 7 days. 184 57

The ESCA study gives a good qualitative and quantitative elemental analysis of internal and external surfaces of foreign materials. Microporous hydrophobic Mitrathane (a polyetherurethane urea) grafts were implanted as blood conduits in dogs for up to 6 months. Surface analysis of explanted grafts demonstrated the presence of different contaminants: sodium, chlorine, silicon, in patent grafts, i.e. those implanted for 1 month and less. The sulphur probably comes from the presence of proteins on the surface of the polymer and the high level of nitrogen is also protein-related. At 6 month implantation, the grafts were occluded and a decrease of proteins on the surface was observed. The values of N/C and O/C ratios are also reported. For the virgin material, these ratios correspond to the quantity of hard and soft segments; but, for the explanted grafts, these parameters are also influenced by the presence of proteins due to the Versaclean washing which did not wash away all the proteins on the surface of the polymer. The SEM photographs showed a certain degradation of polyurethane after 6 month of implantation. However, by ESCA study, it is difficult to compare the surface of virgin and explanted grafts because it is masked by the presence of proteins.
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PMID:Hydrophobic and fibrillar microporous polyetherurethane urea prosthesis: an ESCA study on the internal and external surfaces of explanted grafts. 260 85

We analyzed biochemical data derived from 911 patients with renal insufficiency observed at our institution for periods up to 7 years. During early renal failure (RF) (creatinine less than 5 mg/dL), the rate of change of hematocrit, total CO2 (tCO2) and urea per unit change of creatinine was significantly higher than during moderate (creatinine between 5 and 10 mg/dL) or advanced (creatinine greater than 10 mg/dL) RF. For example, the rate of change of hematocrit (%, volume/volume [v/v]) was (mean +/- SEM) -2.15 +/- 0.15% for each 1 mg/dL increase in creatinine in the range of creatinine less than 5 mg/dL, whereas for the range of creatinine greater than 10 mg/dL, the rate of change was only -0.48 +/- 0.06% (P less than 0.001). Similarly, the rate of change of tCO2 was -1.68 +/- 0.09 mEq/L for each 1 mg/dL increment in creatinine concentration during early RF, and -0.19 +/- 0.09 mEq/L per unit increase in creatinine during advanced RF (P less than 0.001). Chloride concentration initially increased as a function of creatinine in early RF, but decreased in advanced RF, whereas the anion gap increased throughout the course of RF. Mean serum phosphate concentration also increased steadily, but remained below the upper range of normal (4.7 mg/dL) during early RF without the use of phosphate binders. These data suggest that different biochemical parameters change at different rates as a function of the severity of renal dysfunction, and that although phosphate retention may occur, hyperphosphatemia is not a hallmark of early RF.
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PMID:Biochemical parameters in chronic renal failure. 312 41

In the present study we used the pH sensitive absorbance of 5(and6)-carboxy-4',5'-dimethylfluorescein to investigate intracellular pH (pHi) regulation in A10 vascular smooth muscle cells: (1) The steady state pHi in A10 cells averaged 7.01 +/- 0.1 (mean +/- SEM, n = 26) at an extracellular pH of 7.4 (28 mM HCO3/5% CO2). (2) Removal of extracellular sodium led to an intracellular acidification of 0.36 +/- 0.07 pH-units (mean +/- SEM, n = 8). (3) pHi-Recovery after an acute intracellular acid load (by means of NH4Cl-prepulse) was reversibly blocked by 1 mM amiloride and was dependent on the presence of sodium. The velocity of pHi recovery increased with increasing sodium concentrations with an apparent Km for external sodium of about 30 mM and a Vmax of about 0.35 pH units/min. These findings are compatible with a Na/H exchanger being responsible for pHi recovery after an acid load. (4) Removal of extracellular chloride induced an intracellular alkalinization of 0.23 +/- 0.03 pH-units (mean +/- SEM, n = 10). The alkalinization was dependent on the presence of extracellular bicarbonate. (5) Removal of chloride during pHi recovery from an alkaline load (imposed by acetate prepulse) stopped and reversed pHi backregulation. Chloride removal had no effect in the absence of bicarbonate or in the presence of 10(-4) M DIDS, suggesting that the effects were mediated by a Cl/HCO3 exchanger. In conclusion we have demonstrated evidence for a Na/H exchanger and a Cl/HCO3 exchanger in A10 vascular smooth muscle cells.
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PMID:Evidence for Na/H exchange and Cl/HCO3 exchange in A10 vascular smooth muscle cells. 317 85

The effect of long-term gentamicin administration on sodium, potassium, chloride and phosphorus concentrations was studied in individual rat renal tubular cells using electron microprobe analysis. Histological damage was apparent only in proximal tubular cells. The extent of damage was only mild after 7 days of gentamicin administration (60 mg/kg body wt/day) but much more pronounced after 10 days. GFR showed a progressive decline during gentamicin treatment. In non-necrotic proximal tubular cells, sodium was increased from 14.6 +/- 0.3 (mean +/- SEM) in controls to 20.6 +/- 0.4 after 7 and 22.0 +/- 0.8 mmol/kg wet wt after 10 days of gentamicin administration. Chloride concentration was higher only after 10 days (20.6 +/- 0.6 vs. 17.3 +/- 0.2 mmol/kg wet wt). Both cell potassium and phosphorus concentrations were diminished by 6 and 15, and by 8 and 25 mmol/kg wet wt after 7 and 10 days of treatment, respectively. In contrast, no major alterations in distal tubular cell electrolyte concentrations could be observed after either 7 or 10 days of gentamicin administration. As in proximal tubular cells, distal tubular cell phosphorus concentrations were, however, lowered by gentamicin treatment. These results clearly indicate that gentamicin exerts its main effect on proximal tubular cells. Decreased potassium and increased sodium and chloride concentrations were observed in proximal tubular cells exhibiting only mild histological damage prior to the onset of advanced tissue injury. Necrotic cells, on the other hand, showed widely variable intracellular electrolyte concentration patterns.
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PMID:Electrolyte composition of renal tubular cells in gentamicin nephrotoxicity. 340 11

A method of measuring total body chlorine (TBCl) by prompt gamma in vivo neutron activation analysis is described which depends on the same NaI(Tl) spectra used for determinations of total body nitrogen. From these spectra counts ratios of chlorine to hydrogen are derived and TBCl is determined using a model of body composition which depends on measured body weight, total body water (by tritium dilution) and protein (6.25 X nitrogen) as well as estimated body minerals and glycogen. The precision of the method based on scanning an anthropomorphic phantom is at present only approximately 9% (SD), for a patient dose equivalent of less than 0.30 mSv. Spectra collected from 67 normal volunteers (32 male, 35 female) yielded mean values of TBCl of 72 +/- 19 (SD) g in males and 53.6 +/- 15 g in females, in broad agreement with values reported by workers using delayed gamma methods. Results are also presented for two human cadavers analysed both by neutron activation and by conventional chemical analysis; the ratios of TBCl (neutron activation) to TBCl (chemical) were 0.980 +/- 0.028 (SEM) and 0.91 +/- 0.09. Finally, it is suggested that an improvement in precision will be achieved by increasing the scanning time (thereby increasing the radiation dose equivalent) and by adding two more detectors.
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PMID:Measurement of total body chlorine by prompt gamma in vivo neutron activation analysis. 356 33

To further delineate the effects of fasting and sodium deprivation on the handling of sodium when sodium intake is resumed, balance studies were performed on seven obese female subjects. All subjects underwent a period of total fasting, which continued for 27 to 29 days prior to resumption of sodium intake. Natriuresis in the first week of fasting and continued sodium chloride deprivation resulted in cumulative deficits of 383 +/- 47 mEq (SEM) and 371 +/- 41 mEq of sodium and chloride, respectively. Chloride space decreased from 21.2 +/- 2.7 L to 18.7 +/- 2.5 L, and aldosterone secretory rates (ASR) increased from 43 +/- 13 micrograms/24 h to 597 +/- 138 micrograms/24 h. Following resumption of sodium intake and simultaneous refeeding on low calorie diets in studies on four subjects (group I), cumulative sodium balances during the first seven days ranged from +586 mEq to +1,109 mEq; sodium retained/previously existing sodium deficit = 2.4, 3.2, 2.0, and 1.6 in the four subjects, respectively. Continued sodium retention resulted in cumulative sodium balances ranging from +670 mEq to +1,249 mEq at the end of 19 to 22 days in studies on three subjects whose cumulative sodium balance was +1,249 mEq, sodium retained/sodium deficit = 3.6. During the first five days of sodium intake and refeeding ASR decreased to 74 +/- 26 micrograms/24 h. Sodium chloride administration without refeeding in studies on three subjects (group II) also resulted in retention of more than enough sodium to replenish previously existing sodium deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of marked and persistent sodium retention in previously fasted and sodium-deprived obese subjects. 360 Feb 74

A sample of 165 extracted or exfoliated teeth containing amalgam restorations were categorized as to the degree of marginal integrity of the amalgam. Microstructures of the samples representing the highest (grade 11) and lowest (grades 1 and 2) degrees of marginal deterioration were studied by SEM/EDS. The clinical evaluation and microscopic evaluation indicated that samples showing poor marginal integrity contained large quantities of tin-rich and tin-chlorine-rich corrosion products with little or no gamma-2 phase remaining. Obvious signs of fracture and cracking at the cavosurface were always present. Products containing calcium were extensively associated with corrosion products containing tin, and these were found predominantly at the tooth-amalgam interface. No copper-rich amalgams were found in this grouping. Amalgams with good marginal integrity had no microscopic cracks or fractures and generally little evidence of corrosion was found. However, one of six samples had extensive corrosion products, indicating that corrosion product formation is not the only factor contributing to marginal deterioration. After 6 years of clinical use, the degree of marginal deterioration did not appear to depend unerringly on time of use. Further work is necessary to define the microstructural characteristics of samples showing intermediate amounts of marginal deterioration and to determine if copper-rich amalgams consistently have small to moderate amounts of marginal deterioration.
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PMID:Characteristics of amalgam restorations with variable clinical appearance. 385 63


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