Disease relevance of dysprosium

• Treatment of rheumatoid synovitis of the knee with intraarticular injection of dysprosium 165-ferric hydroxide macroaggregates [1].
• Delineation of acute myocardial infarction with dysprosium DTPA-BMA: influence of dose of magnetic susceptibility contrast medium [2].
• PURPOSE: To use (a) dysprosium-based contrast agent (sprodiamide) to confirm the site of myocardial injection and (b) T1-enhancing magnetic resonance (MR) contrast media to mark the myocardial target and T2*-enhancing contrast media to demonstrate injection sites in the margins or core of infarction on delayed contrast-enhanced images [3].
• Toxicity of dysprosium shift reagents in the isolated perfused rat kidney [4].
• Early detection of perfusion deficits caused by regional cerebral ischemia in cats. T2-weighted magnetic susceptibility MRI using a nonionic dysprosium contrast agent [5].

Psychiatry related information on dysprosium

• After overnight food deprivation, they were fed a test meal labeled 67Zn-CPP or 67ZnCl2 (4 g Zn-free diet + 0.12 mg 67Zn) with 0.5 mg Dysprosium (Dy) as a fecal marker [6].

High impact information on dysprosium

• One hundred eight knees of 93 patients with seropositive rheumatoid arthritis and persistent synovitis of the knee were treated with an intraarticular injection of 270 mCi of dysprosium 165 bound to ferric hydroxide macroaggregate [1].
• 23Na spectra in the presence of a paramagnetic shift reagent (dysprosium tripolyphosphate) consisted of two resonances, an unshifted one corresponding to intracellular Na+ and a shifted one corresponding to Na+ in the extracellular medium, including the periplasm [7].
• 23Na NMR, in combination with an anionic paramagnetic shift reagent dysprosium bis(tripolyphosphate), has been used to study intracellular Na+ in Rana oocytes, ovulated eggs, and early cleavage embryos [8].
• The anionic frequency shift reagent, dysprosium (III) tripolyphosphate, which does not permeate intact cells, when added to suspensions of intact adult rat cardiac myocytes, alters the NMR frequency of extracellular sodium ions, [Na+]o, leaving that of intracellular ions, [Na+]i, unaffected [9].
• Isotope ratios were measured in urine and feces, and total zinc and dysprosium were measured in fecal samples [10].

Chemical compound and disease context of dysprosium

• In vitro and in vivo dissolution behavior of a dysprosium lithium borate glass designed for the radiation synovectomy treatment of rheumatoid arthritis [11].
• Comparison of dysprosium DTPA BMA and superparamagnetic iron oxide particles as susceptibility contrast agents for perfusion imaging of regional cerebral ischemia in the rat [12].
• The combination of the two contrast media may define reperfusion of the myocardium at the tissue level (Gadolinium distribution) and the presence and extent of myocardial necrosis (diminished dysprosium effect) in reperfused myocardial infarctions [13].

Biological context of dysprosium

• Dysprosium as a nonabsorbable fecal marker in studies of zinc homeostasis [10].
• Dysprosium-loaded cells might be useful in the study of perfusion and tissue blood volume [14].
• The uptake of Li into the cells was followed as a function of solution conditions, temperature, hematocrit, and blood age using dysprosium tripolyphosphate shift reagent [15].
• Gd chelates are predominantly dipolar relaxation enhancers, whereas Dy chelates are efficient susceptibility agents only in compartmentalized systems [16].
• Kinetics of [103Ru]phenanthroline and dysprosium particulate markers in the rumen of steers [17].

Anatomical context of dysprosium

• PURPOSE: To show the effect of dysprosium diethylenetriaminepentaacetic acid bis-methylamine injection on the images of normal human myocardium [18].
• The cytosol of intact human red blood cells was loaded with 28.1 +/- 3.4 mM of dysprosium DTPA-BMA using a hypoosmotic technique [14].
• 23Na NMR experiments with a suspension of the renal epithelial cell line, LLC-PK1/Cl4, in the presence of the shift reagent dysprosium polyphosphate showed that the intracellular sodium was only NMR visible for 64 +/- 4% [19].
• The slope (k) of R*(2) vs. tissue dysprosium concentration in sec(-1) mM(-1) for myocardium was 97.1 (95% C.I. 77. 0-117.2), liver 122.6 (108.3-136.9), spleen 22.5 (8.8-36.3), kidney 68.1 (58.6-77.6), and skeletal muscle 77.9 (4.1-151.6); k was significantly different (P < 0.05) for all pairings except those with skeletal muscle [20].
• The effects of two widely used paramagnetic shift reagents for cationic NMR, dysprosium tripolyphosphate [Dy(PPP)2(7-)] and dysprosium triethylenetetramine hexaacetate [Dy(TTHA)3-], on the cell structure of dog and human erythrocytes, dog kidney cortical tubules and rat hepatocytes were investigated [21].

Associations of dysprosium with other chemical compounds

• During NMR studies, the serosal bath consisted of aerated 2.4 mM HCO3 amphibian Ringer's (pH 8.1) made up with 15% D2O containing the shift reagent, dysprosium tripolyphosphate (1 mM) [22].
• The DyLB microspheres reacted nonuniformly in SSF with the majority of lithium and boron being dissolved, whereas nearly all of the dysprosium (>99.7%) remained in the reacted microspheres [11].
• Sequential equimolar doses of 0.1, 0.3, and 0.5 mmol/kg of ionic dysprosium diethylenetriamine pentaacetic acid dimeglumine ([NMG]2DyDTPA) or nonionic dysporosium diethylenetriamine pentaacetic acid-bis-methylamide (DyDTPA-BMA) (sprodiamide injection) were administered intravenously into the left jugular vein as a bolus [23].
• RATIONALE AND OBJECTIVES: Gadolinium (Gd) and dysprosium (Dy) analogues, chelated with HP-DO3A, were compared at both 0.5- and 1.0-mol/L concentrations for efficacy in first-pass brain studies on magnetic resonance (MR) imaging at 1.5 tesla (T) [24].
• Masticated boli and wet-sieved masticated leaves (ML) and stems (MS) retained by a 4.0-mm sieve and feces retained by a .063-mm sieve were mordanted with chromium or marked with erbium, ytterbium, or dysprosium, respectively [25].

Gene context of dysprosium

• Incubation with Dy3+, PPP5- or Dy(TTHA)3- caused little or no structural effects but dysprosium was found to penetrate slowly inside tubules with Dy(TTHA)3-. Both Dy3+ and Dy(PPP)2(7-) penetrated rapidly inside cells [21].
• Based on the concentration-dependent effect of dysprosium on the lifetime of cytochrome c, it is possible to make distance estimates from the EPR active center to Dy3+ [26].
• Some of the lanthanides, the rare earth metals, lanthanum (La), cerium (Ce), neodymium (Nd), samarium (Sm), terbium (Tb), dysprosium (Dy), erbium (Er) and ytterbium (Yb) prolonged the clotting time of normal human plasma in a dose-dependent manner when clotting was induced either by thromboplastin or by kaolin in the presence of cephalin and Ca2+ [27].

Analytical, diagnostic and therapeutic context of dysprosium

• Sequential echo-planar imaging was then used in conjunction with bolus injections of the magnetic susceptibility contrast agent, dysprosium DTPA-BMA, to characterize the underlying cerebrovascular perfusion deficits [28].
• Neutron activation analysis with dysprosium as a tracer was employed to determine quantitatively the microleakage around the restorations of an experimental hydrophobic composite, as well as a commercial composite [29].
• The intracellular sodium concentration [( Na+]i) of dog kidney cortical tubules was monitored by flame photometry and 23Na NMR using dysprosium tripolyphosphate as shift reagent [30].
• The proximal tubules were then purified and concentrated by Percoll density gradient centrifugation and then resuspended in buffer containing dysprosium tripolyphosphate shift reagent [31].
• The curves for tissue signal intensity versus time during first pass return artifactually to near baseline after Gd chelate injection (when SSFP imaging techniques are used), a differentiating feature from results with the Dy chelate [24].

References