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)

The intracellular pH (pHi) of tissue-cultured bovine lens epithelial cells was measured in small groups of 6 to 10 cells using the trapped fluorescent dye 2',7'-bis-(2-,carboxyethyl)-5 (and 6)carboxyfluorescein (BCECF). When perifused at 35 degrees C with artificial aqueous humour solution (AAH) containing 16 mM HCO3- and 5% CO2, pH 7.25, pH(i) was 7.19 +/- 0.02 (SEM, n = 95). On removing HCO3- and CO2 there was an initial transient alkalinization followed by a fall in pH to a steady value of 6.97 +/- 0.03 (SEM, n = 54). Addition of 0.25 mM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) to AAH containing HCO3- and CO2 led to a rapid and pronounced fall in pH. Exposure to Na(+)-free AAH again led to a marked fall in pH(i), but in this case the addition of DIDS did not produce a further fall. Substitution of the impermeant anion gluconate for Cl- in the presence of HCO3- led to a rise in pHi, while substitution in the absence of HCO3- led to a fall in pHi. The above data indicate a significant role for a sodium-dependent Cl(-)-HCO3- exchange mechanism in the regulation of pHi. Addition of 1 mM amiloride to control AAH in both the presence and absence of HCO3- led to a marked fall in pH(i), indicating that a Na+/H+ exchange mechanism also has a significant role in the regulation of pHi.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:pH regulation in tissue-cultured bovine lens epithelial cells. 133 65

Slip cast conical implants of HA, carbonate-HA, calcium orthophosphate/hydroxyapatite and hydroxyapatite/calcium pyrophosphate/calcium orthophosphate with weight ratios 75/25 and 50/30/20 were implanted in rabbit tibia. The bone-implant interfaces were evaluated histologically, by means of SEM/EDX analysis and by push-out test. Thirty-six implanted samples were investigated after 2, 8, and 24 weeks. The triphasic calcium phosphate showed a moderate disintegration. This material showed 2 weeks after implantation a bonding between new bone and implant could be seen in parts of the operation site by SEM. Eight weeks after implantation an intimate relationship between the bone tissue and all specimens of each material was found. After 24 weeks the Ca/P ratio in the bone had reached the Ca/P ratio of mature bone determined by SEM/EDX analysis.
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PMID:Reaction of bone to HA, carbonate-HA, hydroxyapatite + calcium orthophosphate and to hydroxyapatite + calcium ortho- and pyrophosphate. 133 68

Intracellular pH (pHi) of cultured bovine trabecular cells was measured using video-imaging techniques with a pH-sensitive intracellular fluorescent dye, BCECF. In bicarbonate-rich Ringer at pH 7.4, pHi was 7.29 +/- 0.03 (+/- SEM, n = 12 monolayers, 120 cells sampled). Exposure to 20 mM NH4Cl immediately alkalinized pHi: replacement with a Na(+)-rich solution acidified pHi before recovery to resting levels. When NH4Cl was replaced by a low Na+ solution, acidification was sustained but pHi recovery occurred after Na(+)-rich solution. A pHi of 7.11 +/- 0.02 (n = 2 monolayers, 20 cells) occurred in pH 6.8 and pHi was 7.72 +/- 0.03 (n = 2 monolayers, 20 cells) in pH 8.0. Amiloride (1 mM) acidified pHi but DIDS (1 mM) treatment, HCO3(-)-free condition, 1 mM ouabain, 50 mM K+, and 2 mM BaCl2 failed to change pHi. Hydrogen peroxide (1 mM) acidified pHi but no change occurred with 50 microM. Trabecular cells possess an Na+/H+ exchanger similar to that in other cell types.
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PMID:Intracellular pH regulation by a Na+/H+ exchanger in cultured bovine trabecular cells. 133 29

There is a growing evidence that central nervous system chloride transport via gamma-aminobutyric acid (GABAA) related Cl- conductance or Cl-/HCO3- exchange affects anesthetic requirements. To delineate the effects of GABAA-related Cl- conductance blockade versus Cl-/HCO3- exchange inhibition, we determined the change in minimum alveolar anesthetic concentration (MAC) of halothane in rats after intracisternal infusion of 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene (DIDS). DIDS inhibits Cl-/HCO3- exchange transport in concentrations greater than 1 microM and in GABAA-related Cl- channels in concentrations greater than 0.1 mM. After control MAC determination, rats were given intracisternal mock cerebrospinal fluid (n = 6), 1.0 microM DIDS (n = 8), or 1 mM DIDS (n = 8) at a rate of 2 microL/min for 30 min. Mock cerebrospinal fluid did not change the MAC of halothane. The MAC of halothane increased significantly (P less than 0.001) from 0.96% +/- 0.02% to 1.11% +/- 0.03% (mean value +/- SEM) with 1 microM DIDS and from 0.94% +/- 0.02% to 1.16% +/- 0.04% with 1 mM DIDS. The increases in MAC with 1 microM and 1 mM DIDS were not statistically different. This suggests that Cl-/HCO3- exchange inhibition increases halothane requirements, whereas GABAA-related Cl- channel blockade does not.
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PMID:Effect of chloride transport blockade on the MAC of halothane in the rat. 161 35

This study was undertaken to evaluate the effects of dietary K intake, independent of whether the accompanying anion is Cl- or HCO3-, on urinary Ca excretion in healthy adults. The effects of KCl, KHCO3, NaCl and NaHCO3 supplements, 90 mmol/day for four days, were compared in ten subjects fed normal constant diets. Using synthetic diets, the effects of dietary KCl-deprivation for five days followed by recovery were assessed in four subjects and of KHCO3-deprivation for five days followed by recovery were assessed in four subjects. On the fourth day of salt administration, daily urinary Ca excretion and fasting UCa V/GFR were lower during the administration of KCl than during NaCl supplements (delta = -1.11 +/- 0.28 SEM mmol/day; P less than 0.005 and -0.0077 +/- 0.0022 mmol/liter GFR; P less than 0.01), and lower during KHCO3 than during control (-1.26 +/- 0.29 mmol/day; P less than 0.005 and -0.0069 +/- 0.0019 mmol/liter GFR; P = 0.005). Both dietary KCl and KHCO3 deprivation (mean reduction in dietary K intake -67 +/- 8 mmol/day) were accompanied by an increase in daily urinary Ca excretion and fasting UCaV/GFR that averaged on the fifth day +1.31 +/- 0.25 mmol/day (P less than 0.005) and +0.0069 +/- 0.0012 mmol/liter GFR (P less than 0.005) above control. Both daily urinary Ca excretion and fasting UCaV/GFR returned toward or to control at the end of recovery. These observations indicate that: 1) KHCO3 decreases fasting and 24-hour urinary Ca excretion; 2) KCl nor NaHCO3, unlike NaCl, do not increase fasting or 24-hour Ca excretion and 3) K deprivation increases both fasting and 24-hour urinary Ca excretion whether the accompanying anion is Cl- or HCO3-. The mechanisms for this effect of K may be mediated by: 1) alterations in ECF volume, since transient increases in urinary Na and Cl excretion and weight loss accompanied KCl or KHCO3 administration, while persistent reductions in urinary Na and Cl excretion and a trend for weight gain accompanied K deprivation; 2) K mediated alterations in renal tubular phosphate transport and renal synthesis of 1.25-(OH)2-vitamin D, since KCl or KHCO3 administration tended to be accompanied by a rise in fasting serum PO4 and TmPO4 and a fall in fasting UPO4 V/GFR, a fall in serum 1,25-(OH)2-D and a decrease in fasting UCa V/GFR, while dietary KCl or KHCO3 deprivation were accompanied by a reverse sequence.
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PMID:Potassium administration reduces and potassium deprivation increases urinary calcium excretion in healthy adults [corrected]. 164 46

Epithelial cell height was measured in order to estimate the cell volume of dark cells from the ampullae of the semicircular canal of the gerbil. Under control conditions, addition of 10(-4) mol/l piretanide, 10(-5) mol/l 5-nitro-2(3-phenylpropylamino)-benzoic acid (NPPB), 5 mmol/l barium or 10(-3) mol/l quinidine had no significant effect on cell height. Addition of 10(-4) mol/l NPPB or 10(-3) mol/l ouabain led to a small significant decrease in cell height which was not reversible. Substitution of Na+ by N-methyl-D-glucamine or of Cl- by gluconate led to a significant and reversible reduction in cell height. Isotonic elevation of [K+] from 3.6 to 25 mmol/l in a PO4-buffered, HCO3-free solution led to an increase in cell height from 5.8 +/- 0.1 (SEM) to 8.7 +/- 0.2 microns (n = 62) during the first 40 s. During prolonged exposure to elevated [K+] (3-5 min; n = 19), some tissue samples underwent a regulatory volume decrease. K(+)-induced swelling was absent in both isotonic Cl(-)-free and isotonic Na(+)-free solutions and was inhibited by the loop diuretic piretanide (10(-5) and 10(-4) mol/l) or by the (Na+ + K+) ATPase inhibitor ouabain (10(-3) mol/l) or by 10(-4) mol/l NPPB. After the removal of ouabain or 10(-4) mol/l NPPB, K(+)-induced swelling under control conditions was enhanced and was less reversible as compared to control conditions before the experiment. K(+)-induced swelling was not altered by NPPB (10(-5) mol/l) or barium (5 mmol/l); however, barium slowed shrinking upon return of [K+] to control level. In the presence of 10(-3) mol/l quinidine, K(+)-induced swelling was enhanced and not reversible. These data suggest that dark cells from the semicircular canal possess an Na+2Cl-K+ cotransporter as a solute uptake mechanism and a solute efflux mechanism which is sensitive to barium and inhibited by quinidine.
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PMID:K(+)-induced swelling of vestibular dark cells is dependent on Na+ and Cl- and inhibited by piretanide. 169 72

The tolerance of the duodenal mucosa to luminal acid was investigated by measuring with a liquid sensor pH microelectrode technique the epithelial surface pH (pHs) and subepithelial tissue pH (pHt) in rat proximal (duodenal bulb, Brunner gland area) and distal duodenum exposed to luminal acid. Under basal conditions, pHs was roughly equal in both parts of the duodenum; proximal duodenum, 7.40 +/- 0.14 (mean +/- SEM) at the villus tip and 7.54 +/- 0.16 at the depth of crypt; distal duodenum, 7.46 +/- 0.19 and 7.55 +/- 0.09, respectively. Yet, exposure of the mucosa to luminal acid (10 mM HCl) provoked a significantly lesser decrease of pHs (0.25 +/- 0.13 vs 0.42 +/- 0.12 pH units) in the proximal duodenum, suggesting that the response of epithelial HCO3 secretion to luminal acid is stronger in that part of the duodenum. Further, the initial acidification of pHs was followed in the proximal duodenum by a secondary alkalinization of pHs, leading to normalization of pHs, which may suggest activation of compensatory protective mechanisms. pHt at the villus tip was likewise roughly equal in both parts of duodenum (7.29 +/- 0.05 vs 7.17 +/- 0.04), but, again, acidification of the luminal perfusate progressively from 10 to 100 mM HCl induced a much earlier and significantly more profound acidification in the distal than in the proximal duodenum. The possible contribution of Brunner glands to the greater mucosal tolerance to acid in the proximal duodenum was assessed by investigating whether stimulation or inhibition of Brunner gland secretion modulates the response of the duodenal mucosa to acid.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance of rat duodenum to luminal acid. 197 95

The effects of metabolic (bicarbonate, [HCO3]) and respiratory (carbon dioxide, PCO2) acid-base changes on indirectly elicited twitch tension with and without nondepolarizing neuromuscular blocking agents were compared in a rat phrenic nerve-hemidiaphragm preparation. Ionized calcium [Ca2+] and magnesium [Mg2+] concentrations in the modified Krebs' solution were measured and kept constant. Likewise, twitch was altered when pH changes were produced by altering either PCO2 or [HCO3]. Decreasing pH either by increasing PCO2 or by decreasing [HCO3] significantly decreased (P less than 0.01) twitch, by 9.5 +/- 0.6 (SEM, n = 8) and 10.6 +/- 1.5%, respectively. Increasing pH by decreasing PCO2 or by increasing [HCO3] significantly increased (P less than 0.01) twitch, by 5.6 +/- 0.9 and 7.9 +/- 0.6%, respectively. After a partial depression of twitch by nondepolarizing neuromuscular blocking agents, the effects of PCO2 and [HCO3] changes were again assessed. Decreasing pH by increasing PCO2 or by decreasing [HCO3] intensified d-tubocurarine (dTc) (28.2 +/- 1.6 and 32.0 +/- 2.9%, respectively) and vecuronium (23.0 +/- 1.4 and 36.8 +/- 3.2%, respectively) block, whereas it reversed metocurine (1.2 +/- 2.2% NS and 2.9 +/- 1.3%, respectively) and pancuronium (8.3 +/- 1.5 and 11.5 +/- 3.0%, respectively) block. Conversely, increasing pH by decreasing PCO2 or by increasing [HCO3] antagonised dTc (12.8 +/- 2.2 and 13.6 +/- 1.8%, respectively) and vecuronium (25.3 +/- 1.7 and 25.0 +/- 3.0%, respectively) block, whereas it potentiated metocurine (4.2 +/- 0.6 and 8.0 +/- 1.1%, respectively) and pancuronium (11.0 +/- 1.2 and 17.5 +/- 2.0%, respectively) block. Except where indicated, all changes in block described above were statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuromuscular effects of respiratory and metabolic acid-base changes in vitro with and without nondepolarizing muscle relaxants. 153 Dec 87

Although it is recognized that inhalation of acid aerosols by subjects with asthma can cause bronchoconstriction, the effects of the inhalation of an alkaline aerosol are unknown. When supplemental inflatable restraints (automobile air bags) are deployed an alkaline aerosol is released. This aerosol is composed of particles of sodium carbonate and sodium bicarbonate with some sodium hydroxide. The mass median aerodynamic diameter (MMAD) of the aerosol is approximately 1 micron, and the pH of the aerosol is 9.8 to 10.3. A group of 14 volunteer male subjects with mild asthma inhaled increasing concentrations of this aerosol for 20-min periods of mouth-only tidal ventilation. Pulmonary function tests were performed at baseline (preexposure), after inhalation of room air alone (control), and after each period of inhalation of the aerosol. A total of 5 subjects inhaled aerosols at nominal concentrations of 10, 20, and 40 mg/m3, whereas 11 subjects inhaled aerosols concentrations of approximately 30, 60, and 120 mg/m3. The mean changes in FEV1 and specific airways resistance (SRaw) for the 11 subjects who inhaled the higher concentrations (average highest concentration 126.6 +/- 7.5 mg/m3, mean +/- SEM) were -1.4 +/- 1.9 and +17.5 +/- 8.5%, respectively. Neither change in lung function was clinically or statistically significant. We conclude that the inhalation of relatively high concentrations of this alkaline aerosol by subjects with mild asthma does not result in bronchoconstriction.
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PMID:Inhalation of an alkaline aerosol by subjects with mild asthma does not result in bronchoconstriction. 199 Sep 50

The effects of hemodialysis (HD) on the levels of serum amyloid A (SAA), C-reactive protein (CRP) and interleukin-1 beta (IL-1 beta) were studied in 8 patients. Bicarbonate dialysate was used exclusively, and three different membranes, Cuprophan (CU), cellulose acetate (CA), and polymethylmetachrylate (PMMA) were compared. The SAA levels increased significantly with each membrane. With CU, they rose from 4.0 +/- 2.0 (mg/l, mean +/- SEM) to 9.6 +/- 2.8 at 60 min and to 15.0 +/- 4.9 at 240 min. The values with CA were 3.8 +/- 2.1, 15.3 +/- 5.6, and 23.8 +/- 3.9; and with PMMA 2.4 +/- 1.3, 12.1 +/- 5.6, and 12.1 +/- 5.9, respectively. The alterations of SAA neither correlated with the weight loss nor the increase of serum albumin during dialysis. The CRP values showed insignificant changes. The IL-1 beta levels rose with CU from 87 +/-18 (ng/l) to 155 +/- 33 at 60 min and to 172 +/- 47 at 240 min. With CA, the values were 67 +/- 14, 198 +/- 46, and 121 +/- 23, and with PMMA 63 +/- 13, 246 +/- 93, and 211 +/- 86, respectively. These results did not correlate with the effects of the membranes on complement activation. It is concluded that the release of cytokines during HD apparently leads to a rapid synthesis of acute-phase proteins as a sign of inflammation. Thus, SAA may be used as one indicator of the biocompatibility of HD treatment.
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PMID:Acute-phase proteins during hemodialysis: correlations with serum interleukin-1 beta levels and different dialysis membranes. 201 67


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