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)

An 11-year-old female died within hours of accidentally ingesting a solution of copper sulfate. A postmortem blood sample was found to contain 66 micrograms/mL copper. The initial qualitative identification of this poison in the body organs and fluids was by means of SEM-microprobe analysis (SEM-MPA) and X-ray fluorescence (XRF). The samples were quantified by atomic absorption spectrometry.
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PMID:A fatal copper sulfate poisoning. 177 64

We studied the removal of aluminum (Al), iron (Fe), copper (Cu), lead (Pb) and zinc (Zn) with continuous ambulatory peritoneal dialysis, before and after desferrioxamine B (DFO) administration (2 g intravenously) in two patients with chronic renal failure and Al-related osteopathy. Both patients had 4 peritoneal dialysis exchanges (2 liters each) per day. Blood concentrations of Al increased 413% (patient A) and 190% (patient B) after DFO. Patient B had a 15% increase in Fe; other metals remained unchanged. Dialysate efflux Al concentrations had peak post-DFO increments of 761% and 840% in patients 1 and 2, respectively. Peak post-DFO increments in Fe dialysate concentration were 342% and 89.5% in the respective patients. Dialysate/plasma (D/P) concentration ratios of Al increased from pre-DFO levels (mean +/- SEM) of 0.370 +/- 0.048 to 0.523 +/- 0.061 after DFO; similarly, Fe D/P ratios increased from 0.259 +/- 0.053 to 0.446 +/- 0.075 with DFO therapy. These results indicate an increase in the ultrafiltrable proportion of Al and Fe in plasma after DFO administration. During 3 days after DFO, patient 1 had a total removal of Al and Fe of 2.9 mg and 4.9 mg, respectively. Metal removal in patient 2 was 7.6 mg of Al and 2.7 mg of Fe. Peritoneal extraction of other trace metals was minor.
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PMID:Removal of trace metals by continuous ambulatory peritoneal dialysis after desferrioxamine B chelation therapy. 185 29

Oxygen derived radicals contribute to tissue injury in inflammatory bowel disease. We measured the content of superoxide dismutase and metallothionein (two endogenous copper and zinc containing proteins involved in radical scavenging) in intestinal resection specimens from 29 patients with Crohn's disease and 12 patients with ulcerative colitis and compared the concentrations with those obtained in the normal mucosa of a control group of 18 patients with colorectal cancer. The superoxide dismutase content was similar in control mucosa and non-inflamed mucosa from patients with inflammatory bowel disease (mean (SEM) 2.13 (0.10) and 2.24 (0.10) mg/g protein, respectively) but was decreased in inflamed mucosa (1.87 (0.08) mg/g protein, p less than 0.005 v non-inflamed mucosa). The metallothionein content was decreased in non-inflamed inflammatory bowel disease mucosa compared with control mucosa (0.23 (0.03) and 0.36 (0.04) mg/g protein, respectively, p less than 0.02) and a further decrease was found in inflamed mucosa (0.17 (0.02) mg/g protein, p less than 0.001 v control mucosa). No differences were found between Crohn's disease and ulcerative colitis and no significant effect of medication or tissue localisation was noted. These findings might indicate a decreased endogenous intestinal protection against oxygen derived radicals in inflammatory bowel disease which could contribute to the pathogenesis of the disease.
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PMID:Decrease in two intestinal copper/zinc containing proteins with antioxidant function in inflammatory bowel disease. 195 69

Thiazide diuretics, which are often prescribed to treat mild to moderate hypertension, commonly cause an increase in urinary zinc (Zn) excretion. Metabolic interrelationships between Zn and copper (Cu) are known to exist; consequently, Zn might influence Cu levels. This study aims to determine whether or not Cu and Zn levels in hypertensive patients were influenced by treatment with clopamide, a thiazide diuretic. Eight male patients, aged 36-59 and with an average supine diastolic pressure of 95-115 mm Hg, were treated with single daily doses of clopamide 5 mg as monotherapy for 16 weeks. Plasma, erythrocyte (RBC), and mononuclear leukocyte (WBC) levels of Cu and Zn were determined immediately before therapy (week 0) and again at weeks 8 and 16. There was a significant fall in Cu in mononuclear WBCs from 13.25 (SEM = 0.86) to 1.9 fg/cell (SEM = 0.56) (p less than 0.001) and an increase in Zn from 33.87 (SEM = 3.7) to 70.8 fg/cell (SEM = 11.7) (p less than 0.001), with no change in either cell count or measurable cell volume. Plasma Cu levels increased significantly (p less than 0.001), but the Zn levels decreased only slightly (p less than 0.03). Changes in RBC Cu levels during the treatment period were not significantly altered (p less than 0.1). Zn levels in RBCs were significantly (p less than 0.04) lower. It is concluded that treatment with clopamide may induce some changes in Cu and Zn levels in normal hypertensives, particularly in WBCs. Further investigation is needed to determine the extent of this influence.
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PMID:Effect of clopamide, a thiazide diuretic, on copper and zinc levels in hypertensive patients. 201 May 78

Concentrations of copper (Cu) and ceruloplasmin in serum were measured serially in 49 preterm infants with mean (+/- SEM) birth weights of 979 +/- 33 g and gestational ages of 28.4 +/- 0.3 weeks at three, six, nine, and 12 months postpartum. Serial radiographic studies showed 17 infants with (group A) and 32 infants without (group B) rickets or fractures. Cu and ceruloplasmin concentrations in serum also were measured in 21 healthy term infants (group C) with birth weights 3668 +/- 98 g at three, six, and 12 months postpartum. Analyses of covariance of serial changes in these serum variables--taking into account such potential covariates as differences in gestational age, birth weight, initial weight and length, changes in weight and length during the study, the duration of parenteral nutrition, and increased enteral copper intake--showed both groups of preterm infants had significantly lower concentrations of Cu in serum up to age six months and ceruloplasmin up to age three months (P less than 0.001) when compared with term infants. By one year of age, Cu and ceruloplasmin concentrations in serum in all groups had increased significantly (P less than 0.001), into the adult range, and were not significantly different among groups. These data document a maturational lag in copper metabolism in small, preterm infants. Changes in concentrations of Cu and ceruloplasmin in serum were significantly correlated (r = 0.92, P less than 0.001) but were not significantly different between preterm infants with and without rickets or fractures at each age.
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PMID:Sequential concentrations of copper and ceruloplasmin in serum from preterm infants with rickets and fractures. 201 71

The objective of this study was to determine the in vitro corrosion products that resulted from crevice corrosion of low- and high-copper dental amalgams. Specimens were potentiostatically polarized in a chloride-containing electrolyte while set against a PTFE surface to form a crevice. After 16 h, corrosion products were examined by light microscopy, SEM, EDS, and XRD. Analysis showed the presence of three previously reported products [Sn4(OH)6Cl2, SnO, and Cu2O] and a new product, CuCl, which formed on high-copper, gamma 2-free amalgams. Thermodynamic considerations show that CuCl is stable for the reported in vivo potentials of amalgam restorations and the high acidity and high chloride ion concentration associated with crevice corrosion.
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PMID:Crevice corrosion products of dental amalgam. 206 90

The thrombolytic efficacy of recombinant unglycosylated full length single chain urokinase-type plasminogen activator (rscu-PA, saruplase), applied either as single intravenous bolus or as a continuous infusion over 60 minutes, was studied in 5 randomized blinded groups of 5 dogs with combined copper coil induced coronary artery thrombosis and 125I-fibrin labeled femoral vein clots. Infusion of 1 mg/kg recu-PA (group I) induced coronary recanalization in 4 of 5 dogs and 98 +/- 1% (mean +/- SEM) venous clot lysis. Bolus injection of 1 mg/kg recu-PA (group II) caused reflow in 3 of 5 dogs and 88 +/- 5 percent venous clot lysis. Infusion of 0.5 mg/kg rescu-PA (group III) achieved reflow in 3 of 5 dogs and 52 +/- 6% venous clot lysis. Bolus injection of 0.5 mg/kg rscu-PA (group IV) induced reflow in 4 of 5 dogs and 48 +/- 12% venous clot lysis. Placebo infusion (group V) was associated with late recanalization in 1 of 5 dogs and 18 +/- 8% venous clot lysis. Coronary artery reocclusion after reflow was not observed in groups I and II, but occurred in 2 of 3 animals in group III and in 3 of 4 animals in group IV (P = .02). The time to reflow in responsive animals was 22 +/- 5 minutes with infusion of 0.5 or 1 mg/kg rscu-PA and 14 +/- 1 minute with bolus injection of 0.5 or 1 mg/kg (P = .14). Depletion of fibrinogen and alpha 2-antiplasmin to less than 25% of baseline levels was observed in the 5 dogs given 1 mg/kg rscu-PA by bolus and in 3 of the 5 dogs given 1 mg/kg rscu-PA via infusion, but in none of the dogs that received 0.5 mg/kg rscu-PA (P less than .001). Plasma clearance rates were 170 +/- 44 and 230 +/- 30 mL/minute after bolus injection and 190 +/- 47 and 310 +/- 56 mL/minute during infusion of rscu-PA for the 1 mg/kg and 0.5 mg/kg doses respectively. Thus, intravenous bolus injection of rscu-PA (saruplase) appears to be equipotent to an infusion over 60 minutes for both coronary and venous thrombolysis. This animal model of combined arterial and venous thrombolysis may be useful for the evaluation of new thrombolytic strategies.
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PMID:Comparison of intravenous bolus injection or continuous infusion of recombinant single chain urokinase-type plasminogen activator (saruplase) for thrombolysis. A canine model of combined coronary arterial and femoral venous thrombosis. 211 30

We compared a selective thrombin inhibitor (MCI-9038; Argatroban), a thromboxane A2 (TXA2) receptor antagonist (L-670,596) and a serotonin-2 receptor antagonist (ketanserin) for their ability to hasten clot lysis and delay reocclusion in a canine model of femoral arterial thrombosis. Occlusive thrombosis was induced by insertion of a thrombogenic copper coil. Femoral arterial blood flow velocity (FABFV) was monitored directly and continuously by Doppler flowmetry. Thrombolysis was induced with tissue plasminogen activator (t-PA; 0.8 mg/kg, i.v.), starting 60 min after thrombotic occlusion and continued for 90 min. Ten minutes after occlusion, dogs received an intravenous infusion of either vehicle, MCI-9038 (10 micrograms kg-1 min-1), ketanserin (0.1 mg/kg bolus plus 5 micrograms kg-1 min-1), L-670,596 (1 mg/kg bolus plus 17 micrograms kg-1 min-1) or a combination of L-670,596 and ketanserin. All infusions were discontinued 1 h after stopping the t-PA, and were followed by a 30 min observation period. The times to thrombolysis were similar for all treatments (mean +/- SEM = 47 +/- 3; all groups). MCI-9038 prevented reocclusion, defined as permanent cessation of FABFV during the hour after stopping the t-PA. All dogs receiving MCI-9038 reoccluded within 30 min after stopping its infusion (71 +/- 3 min). Reocclusion occurred in all other dogs, except one vehicle-treated dog and a second dog that received L-670,596 plus ketanserin. Vehicle-treated dogs reoccluded within 23 +/- 8 min. Reocclusion was not delayed significantly by ketanserin, L-670,596 or the combination of the two.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of reocclusion by MCI-9038, a thrombin inhibitor, following t-PA-induced thrombolysis in a canine model of femoral arterial thrombosis. 212 37

We have shown that copper amplifies prostaglandin E2 (PGE2) stimulation of luteinizing hormone-releasing hormone (LH-RH) from explants of the median eminence area (MEA) and that this process is calcium-dependent. Since a Ca-cAMP pathway has been implicated in PGE2 action on the LH-RH neuron, in this study we wished to ascertain if copper exerts its effect on the PGE2 receptor or on a postreceptor component involved in PGE2 action. MEA of adult male rats were incubated for 5 min with 200 microM Cu/histidine (CuCl2 mixed with L-histidine at an equimolar ratio) and then incubated for 15 min either with 10 microM PGE2 (Cu/PGE2), 100 microM forskolin (Cu/forskolin), or 1 mM 8-bromoadenosine 3',5'-cyclic monophosphate (Cu/cAMP). Controls were incubated without Cu/histidine or with Cu/histidine alone. Basal release of LH-RH was 4.6 +/- 0.45 pg/15 min per MEA (mean +/- SEM). Net stimulated release during the 15-min exposure to PGE2, forskolin, or 8-bromoadenosine 3',5'-cyclic monophosphate was 3.6 +/- 0.52, 3.1 +/- 0.39, and 1.6 +/- 0.42 pg/15 min per MEA, respectively. Net stimulated release after exposure to Cu/PGE2, Cu/forskolin, or Cu/cAMP was 12.7 +/- 2.2, 9.9 +/- 1.46, and 1.4 +/- 1.9 pg/15 min per MEA, respectively, indicating that copper amplifies the action of PGE2 and forskolin but not cAMP action. When MEA were exposed to a mixture of PGE2 and forskolin for 15 min, the effects of these two secretagogues on LH-RH release were not additive, regardless of whether the MEA were pretreated with Cu/histidine. In contrast to PGE2 and forskolin, copper did not amplify K+ stimulation of LH-RH release and, moreover, when Cu/histidine-treated MEA were exposed to a mixture of PGE2 and 30 mM K+, the effects of these two secretagogues were additive. These results are supportive of the proposition that PGE2 stimulation of LH-RH release is mediated by the Ca-cAMP pathway and that copper amplification of PGE2 action is a postreceptor event.
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PMID:Copper amplification of prostaglandin E2 stimulation of the release of luteinizing hormone-releasing hormone is a postreceptor event. 243 12

The pharmacokinetics and thrombolytic properties of a variant of human tissue-type plasminogen activator (t-PA), obtained by deletion mutagenesis of the NH2-terminal fibronectin-like finger (F) and epidermal growth factor (E) domains, and substitution of the three known glycosylated Asn residues by Gln (t-PA-delta FE3X), were studied in dogs with a copper coil-induced thrombosis of the left anterior descending coronary artery. Bolus injections were given during 2 min to groups of three dogs. Injection of 0.15 mg/kg resulted in peak antigen levels in plasma of 1.58 +/- 0.72 micrograms/ml (mean +/- SEM) and caused reperfusion within 14 +/- 6 min. With 0.075 mg/kg, corresponding values of 0.81 +/- 0.20 micrograms/ml and 31 +/- 15 min were obtained. A bolus of 0.038 mg/kg yielded plasma peak levels of 0.43 +/- 0.20 micrograms/ml but did not cause coronary recanalization within 3 h. A bolus injection of natural t-PA (Mel-t-PA) at a dose of 0.1 mg/kg in four dogs resulted in plasma peak levels of 0.46 +/- 0.09 micrograms/ml and caused partial coronary artery reperfusion within 3 h in one of four dogs (after 31 min). None of these injections caused a significant decrease of the fibrinogen level. Pharmacokinetic parameters for t-PA-delta FE3X were alpha half-life (t1/2) 14-18 min, beta t1/2 72-125 min, and plasma clearance 21-36 ml/min. For Mel-t-PA, the corresponding values were 3 min, 8 min, and 520 ml/min. We conclude that the variant t-PA-delta FE3X has a markedly longer plasma t1/2 than does Mel-t-PA and, when administered as a bolus injection, a higher thrombolytic efficacy.
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PMID:Pharmacokinetics and thrombolytic properties of a nonglycosylated mutant of human tissue-type plasminogen activator, lacking the finger and growth factor domains, in dogs with copper coil-induced coronary artery thrombosis. 245 51


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