The influences of Ce on the microstructure and mechanics performances of Ti-Fe-Mo-Mn-Nb-Zr alloys were studied and presented in this paper. The microstructure of no-Ce Ti-Fe-Mo-Mn-Nb-Zr alloy was thick, long and dendritic, and the microstructure of alloy was fined by Ce. With the increase in Ce wt%, the microstructure became equiaxial gradually. Hardness decreased with the increase in Ce wt%. The compression yield strength became greater with the increasing of Ce wt%, but after the Ce wt% increased to a certian degree, the compression yield strength became smaller with the further increasing of Ce wt%. This phenomenon was explained in the light of bond energy and X-ray diffraction experiment. X-ray diffraction experiment showed that the alloys were beta-Ti.
Alloys ; chemistry ; Biocompatible Materials ; Cerium ; chemistry ; Hardness ; Materials Testing ; Surface Properties ; Titanium ; chemistry

The appearance of dental porcelains is comparable to natural teeth. This study discusses the effect of Y2O3 addition to the fluorescent property of dental porcelains. The composition of dental porcelains contained Y2O3 as the fluorescent agent and base frit. The combinations of Y2O3 added consist of a series with 0.5, 1.0, 1.5, 2.0 and 2.5 wt% respectively, based on the total composition. In the extreme condition, fluorescent agents are added from 5.0 up to 10.0 wt%. In order to enhance the fluorescent property of dental porcelains, an opacifiying agent, cerium oxide (CeO2) was also added to dental porcelains composition. The fluorescent property was determined using Spectroline EF-1400C/F that emits 240 nm wavelength ultraviolet light. The microstructure was examined by Scanning Electron Microscope (SEM). The result shows that, the fluorescent properties displayed are similar to natural teeth when subjected to ultraviolet light. SEM micrograph was able to show the fluorescent agent dispersed in glass phase. Increasing additions of Y2O3 gave the fluorescent properties near to natural teeth.
*Biocompatible Materials ; *Cerium ; Dental Porcelain/*chemical synthesis ; *Esthetics, Dental ; Fluorescence ; *Yttrium

BACKGROUND: In an attempt to investigate the role of oxidants in the activation of phospholipase A2(PLA2) and endogenous oxidative stress in the lung, acute inflammatory lung injury was induced by the instillation of hydrogen peroxide into the trachea of Sprague-Dawley rats. MATERIAL AND METHOD: To prove the hypothesis that released oxidants from neutrophils activate the PLA2 retrogradely, activities of PLA2 and lysoplatelet activating factor acetyltransferase(lysoPAF AT) were assayed 5 hours after instillation of hydrogen peroxide. In addition, to confirm the impairing effects of the activation of PLA2 associated with endogenous oxidative stress, lung weight/body weight ratio(Lx10(-3)/B), protein contents(mg/two lungs) in bronchoalveolar lavage(BAL) were measured. As neutrophilic respiratory burst has been known to play a pivotal role in the genesis of endogenous oxidative stress associated with acute inflammatory lung injury, BAL neutrophils counts and level of lung myelperoxidase(MPO) were measured after hydrogen peroxide insult. Morphological and histochemical studies were also performed to identify the effect of the endogenous oxidative stress. RESULT: Five hours after hydrogen peroxide instillation, lungs showed marked infiltration of neutrophils and increased weight. Protein contents in BAL increased significantly compared to those of normal rats. PLA2 activity was enhanced in the hydrogen peroxide instilled group. Interestingly, the accelerated production of platelet activating factor(PAF) was confirmed by the increased activity of lysoPAF AT in the H2O2 employed lung. Morphologically, light microscopic findings of lungs after instillation of hydrogen peroxide showed atelectasis and infiltration of inflammatory cells, which was thought to be caused by lipid mediators produced by PLA2 activation. In cerium chloride cytochemical electron microscopy, dense deposits of cerrous perhydroxide were identified. In contrast, no deposit of cerrous perhydroxide was found in the normal lung. CONCLUSION: As all these findings were consistent with the lung injury caused by neutrophilic oxidative stress, it is suggested that the activation of PLA2 by oxidants might participate in the genesis of endogenous oxidative stress. Collectively, the positive feedback loop between oxidative stress and PLA2 activation may participate in the pathogenesis of Adult Respiratory Distress Syndrome(ARDS).
Acute Lung Injury* ; Adult ; Animals ; Blood Platelets ; Cerium ; Humans ; Hydrogen Peroxide* ; Hydrogen* ; Lung ; Lung Injury ; Microscopy, Electron ; Neutrophils ; Oxidants ; Oxidative Stress* ; Phospholipases A2* ; Phospholipases* ; Pulmonary Atelectasis ; Rats ; Rats, Sprague-Dawley ; Respiratory Burst ; Trachea

BACKGROUND: Based on the known immunoregulatory functions of moxifloxacin on phagocytes, the therapeutic effect of moxifloxacin on oleic acid (OA)-induced acute lung injury (ALI) was investigated. METHODS: Moxifloxacin (10 mg/kg) was given to male Sprague-Dawley rats that had been given oleic acid (OA, 30 microliter) intravenously. Five hours after OA injection, parameters demonstrating ALI were assessed to measure the effects of moxifloxacin on acute lung injury. RESULTS: The pathological findings of OA-induced ALI's was diminished by moxifloxacin. Through ultrastructural and CeCl3 EM histochemistry, moxifloxacin was confirmed to be effective in decreasing oxidative stress in the lung as well. Indices of ALI, such as lung weight/body weight ratio, protein content in bronchoalveolar lavage fluid, and lung myeloperoxidase were decreased by moxifloxacin. In diaminobenzidine immunohistochemistry, fluorescent immunohistochemistry, and Western blotting of the lung, moxifloxacin had decreased the enhanced expression of secretory phospholipase A2 (sPLA2) by OA. CONCLUSION: We concluded that moxifloxacin was effective in lessening acute inflammatory pulmonary edema caused by OA, by inhibiting the neutrophilic respiratory burst, which was initiated by the activation of sPLA2.
Acute Lung Injury ; Animals ; Aza Compounds ; Blotting, Western ; Bronchoalveolar Lavage Fluid ; Cerium ; Free Radicals ; Humans ; Immunohistochemistry ; Lung ; Male ; Neutrophils ; Oleic Acid ; Oxidative Stress ; Peroxidase ; Phagocytes ; Phospholipases A2, Secretory ; Pulmonary Edema ; Quinolines ; Rats ; Rats, Sprague-Dawley ; Respiratory Burst

During the previous years, with the emerging of nanotechnology, the enormous capabilities of nanoparticles have drawn great attention from researchers in terms of their potentials in various aspects of pharmacology. Cerium oxide nanoparticles (nanoceria), considered as one of the most widely used nanomaterials, due to its tempting catalytic antioxidant properties, show a promising potential in diverse disorders, such as cerebral ischemic stroke (CIS), cancer, neurodegenerative and inflammatory diseases. Overwhelming generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) during cerebral ischemia and reperfusion periods is known to aggravate brain damage via sophisticated cellular and molecular mechanisms, and therefore exploration of the antioxidant capacities of nanoceria becomes a new approach in reducing cerebral ischemic injury. Furthermore, utilizing nanoceria as a drug carrier might display the propensity to overcome limitations or inefficacy of other conceivable neuroprotectants and exhibit synergistic effects. In this review, we emphasize on the principle features of nanoceria and current researches concerning nanoceria as a potential therapeutic agent or carrier in improving the prognosis of CIS.
Antioxidants ; therapeutic use ; Brain Ischemia ; drug therapy ; Cerium ; chemistry ; therapeutic use ; Humans ; Nanoparticles ; chemistry ; therapeutic use ; Neuroprotective Agents ; therapeutic use ; Oxidative Stress ; drug effects ; Reactive Nitrogen Species ; metabolism ; Reactive Oxygen Species ; Stroke ; drug therapy ; pathology

OBJECTIVETo study the biological effects of nanoscale copper oxide (nCuO), zinc oxide (nZnO), cerium dioxide (nCeO2) and their mixtures on Carassius auratus.

METHODSJuvenile fish (Carassius auratus) were exposed to aqueous suspensions of nCuO, nZnO, and nCeO2 (alone and in mixtures) at concentrations of 20, 40, 80, 160, and 320 mg/L. The biomarkers-acetylcholinesterase (AChE) in brain, sodium/potassium-activated ATPase (Na+/K+-ATPase) in gill, and superoxide dismutase (SOD) and catalase (CAT) in liver-were determined after 4 days of exposure. Integrated biomarker response (IBR) was calculated by combining multiple biomarkers into a single value.

RESULTSAChE and SOD activities were significantly inhibited by all test metal oxide nanoparticles (NPs) at high concentrations (⋝160 mg/L) with the exception of nCeO2. Na+/K+-ATPase induction exhibited bell-shaped concentration-response curves. CAT activity was significantly inhibited at concentrations equal to or higher than 160 mg/L. The order of IBR values was nCeO2 ≈ nZnO/nCeO2 ≈ nCuO/nCeO2 < nCuO/nZnO/nCeO2 < nZnO < nCuO < nCuO/nZnO. The joint effect seemed to be synergistic for nCuO/nZnO mixtures, additive for the ternary mixture and less than additive or antagonistic for the binary mixtures containing nCeO2.

CONCLUSIONConcentration-dependent changes of enzymatic activities (AChE, Na+/K+-ATPase, SOD, and CAT) were observed in fish exposed to nanoscale metal oxides. IBR analysis allowed good discrimination between the different exposures and might be a useful tool for the quantification of integrated negative effects induced by NPs toward fish.

Acetylcholinesterase ; metabolism ; Animals ; Biomarkers ; metabolism ; Brain ; drug effects ; enzymology ; Cerium ; toxicity ; Copper ; toxicity ; Gills ; drug effects ; enzymology ; Goldfish ; metabolism ; Liver ; drug effects ; enzymology ; Metal Nanoparticles ; toxicity ; Random Allocation ; Sodium-Potassium-Exchanging ATPase ; metabolism ; Superoxide Dismutase ; metabolism ; Toxicity Tests ; Water Pollutants, Chemical ; toxicity ; Zinc Oxide ; toxicity

AIMTo study the biochemistry of lanthanides, the cooperative action of inorganic and organic anti-tumor drugs.

METHODSA series of rare earth complexes were synthesized with Ln(NO3) 6H2O, Phen and 5-Fu. Their anti-tumor activity was measured by the improved MTT, SRB methods.

RESULTSThe formula of complex Ln[(Phen)2(5-Fu)3(NO3)](NO3)2(Ln = Y, La, Ce, Sm, Gd, Dy, Er; Phen = 1, 10-phenanthroline; 5-Fu = fluorouracil) was characterized by elemental analyses, molar conductivity, IR, TGA, and 13C NMR spectra. The preliminary biological activity studies indicated that Lanthanide complex has strong anti-tumor activity in vitro.

CONCLUSIONThe complex might have anti-tumor cooperation action.

Antineoplastic Agents ; chemical synthesis ; chemistry ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cerium ; chemistry ; Drug Synergism ; Dysprosium ; chemistry ; Erbium ; chemistry ; Fluorouracil ; chemistry ; Gadolinium ; chemistry ; Humans ; Lanthanoid Series Elements ; chemistry ; Lanthanum ; chemistry ; Phenanthrolines ; chemistry ; Samarium ; chemistry ; Structure-Activity Relationship ; Yttrium ; chemistry

OBJECTIVES: With recent advances in nanoparticle manufacturing and applications, potential exposure to nanoparticles in various settings is becoming increasing likely. No investigation has yet been performed to assess whether respiratory tract exposure to cerium oxide (CeO2) nanoparticles is associated with alterations in protein signaling, inflammation, and apoptosis in rat lungs. METHODS: Specific-pathogen-free male Sprague-Dawley rats were instilled with either vehicle (saline) or CeO2 nanoparticles at a dosage of 7.0 mg/kg and euthanized 1, 3, 14, 28, 56, or 90 days after exposure. Lung tissues were collected and evaluated for the expression of proteins associated with inflammation and cellular apoptosis. RESULTS: No change in lung weight was detected over the course of the study; however, cerium accumulation in the lungs, gross histological changes, an increased Bax to Bcl-2 ratio, elevated cleaved caspase-3 protein levels, increased phosphorylation of p38 MAPK, and diminished phosphorylation of ERK-1/2-MAPK were detected after CeO2 instillation (p<0.05). CONCLUSIONS: Taken together, these data suggest that high-dose respiratory exposure to CeO2 nanoparticles is associated with lung inflammation, the activation of signaling protein kinases, and cellular apoptosis, which may be indicative of a long-term localized inflammatory response.
Animals ; Apoptosis/*drug effects ; Caspase 3/metabolism ; Cerium/chemistry ; Inflammation ; Lung/*drug effects/metabolism/pathology ; Male ; Metal Nanoparticles/chemistry/*toxicity ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/*drug effects ; bcl-2-Associated X Protein/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism