Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluoridation in Israel was first mooted in 1973 and finally incorporated into law in November 2002 obligating the Ministry of Health to add fluoride to the nation's water supply. Epidemiology studies in the USA have shown that the addition of one part per million of fluoride to the drinking water reduced the caries rate of children's teeth by 50% to 60% with no side effects. Both the WHO in 1994 and the American Surgeon General's report of 2000 declared that fluoridation of drinking water was the safest and most efficient way of preventing dental caries in all age groups and populations. Opposition to fluoridation has arisen from "antifluoridation" groups who object to the "pollution" of drinking water by the addition of chemicals and mass medication in violation of the "Patient's Rights" law and the Basic Law of Human Dignity and Liberty. A higher prevalence of hip fractures in elderly osteoporotic women and osteosarcoma in teenagers has been reported in areas where excess fluoride exists in the drinking water. However, none of the many independent professional committees reviewing the negative aspects of fluoridation have found any scientific evidence associating fluoridation with any ill-effects or health problems. In Israel, where dental treatment is not included in the basket of Health Services, fluoridation is the most efficient and cheapest way of reducing dental disease, especially for the poorer members of the population.
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PMID:[Water fluoridation and public health]. 1463 5

Hydroxyapatite (HA) and gelatin composites were fabricated in a foam type via a novel freeze-drying and crosslinking technique. The morphological and mechanical properties of and in vitro cellular responses to the foams were investigated. The HA powder was added at up to 30 wt % into the gelatin solution, and the mixtures were freeze-dried and further crosslinked. The pure gelatin foam had a well-developed pore configuration with porosity and pore size of approximately 90% and 400-500 microm, respectively. With HA addition, the porosity decreased and pore shape became more irregular. The HA particulates, in sizes of about 2-5 microm, were distributed within the gelatin network homogeneously and made the framework surface rougher. All the foams had high water absorption capacities, showing typical hydrogel characteristics, even though the HA addition decreased the degree of water absorption. The HA addition made the foam much stronger and stiffer (i.e., with increasing HA amount the foams sustained higher compressive stress and had higher elastic modulus in both dry and wet states). The osteoblast-like human osteosarcoma cells spread and grew actively on all the foams. The cell proliferation rate, quantified indirectly on the cells cultured on Ti discs coated with gelatin and gelatin-HA composites using MTT assay, exhibited an up-regulation with gelatin coating compared with bare Ti substrate, but a slight decrease on the composite coatings. However, the alkaline phosphatase activities expressed by the cells cultured on composites foams as well as their coatings on Ti discs were significantly enhanced compared with those on pure gelatin foam and coating. These findings suggest that the gelatin-HA composite foams have great potential for use as hard tissue regeneration scaffolds.
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PMID:Hydroxyapatite and gelatin composite foams processed via novel freeze-drying and crosslinking for use as temporary hard tissue scaffolds. 1554 83

The standard pharmacokinetic model for the analysis of MRI contrast reagent (CR) bolus-tracking (B-T) data assumes that the mean intracellular water molecule lifetime (tau(i)) is effectively zero. This assertion is inconsistent with a considerable body of physiological measurements. Furthermore, theory and simulation show the B-T time-course shape to be very sensitive to the tau(i) magnitude in the physiological range (hundreds of milliseconds to several seconds). Consequently, this standard model aspect can cause significant underestimations (factors of 2 or 3) of the two parameters usually determined: K(trans), the vascular wall CR transfer rate constant, and v(e), the CR distribution volume (the extracellular, extravascular space fraction). Analyses of animal model data confirmed two predicted behaviors indicative of this standard model inadequacy: (1) a specific temporal pattern for the mismatch between the best-fitted curve and data; and (2) an inverse dependence of the curve's K(trans) and v(e) magnitudes on the CR dose. These parameters should be CR dose-independent. The most parsimonious analysis allowing for realistic tau(i) values is the 'shutter-speed' model. Its application to the experimental animal data essentially eliminated the two standard model signature inadequacies. This paper reports the first survey for the extent of this 'shutter-speed effect' in human data. Retrospective analyses are made of clinical data chosen from a range of pathology (the active multiple sclerosis lesion, the invasive ductal carcinoma breast tumor, and osteosarcoma in the leg) that provides a wide variation, particularly of K(trans). The signature temporal mismatch of the standard model is observed in all cases, and is essentially eliminated by use of the shutter-speed model. Pixel-by-pixel maps show that parameter values from the shutter-speed analysis are increased by more than a factor of 3 for some lesion regions. This endows the lesions with very high contrast, and reveals heterogeneities that are often not seen in the standard model maps. Normal muscle regions in the leg allow validation of the shutter-speed model K(trans), v(e), and tau(i) magnitudes, by comparison with results of previous careful rat leg studies not possible for human subjects.
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PMID:Evidence for shutter-speed variation in CR bolus-tracking studies of human pathology. 1557 8

Cobalt(II) complexes with 6-(2-hydroxybenzylamino)purine (HL1), 6-(2-methoxybenzylamino)purine (HL2), 6-(3-methoxybenzylamino)purine (HL3) and 6-(4-methoxybenzylamino)purine (HL4) of the composition [Co(L1)Cl(H2O)2].H2O (1), [Co(L2)Cl(H2O)2] (2), [Co(L3)2(H2O)2].2H2O (3), [Co(L4)2(H2O)2].2H2O (4) have been synthesized. The compounds have been characterized by elemental analysis, FT-IR, ES+ MS (electrospray mass spectra in the positive ion mode) and electronic spectroscopies, magnetic and conductivity data as tetrahedral high-spin cobalt(II) complexes. The thermal stability of the complexes has also been studied. The cytotoxicity of the complexes (1-4) was determined by a Calcein acetoxymethyl (AM) assay. Human malignant melanoma (G361), human chronic myelogenous erythroleukemia (K562), human osteogenic sarcoma (HOS) and human breast adenocarcinoma (MCF7) cell lines were used for the testing. The molecular structure of 6-(3-methoxybenzylamino)purinium chloride monohydrate, H2L3+.Cl.H2O, i.e. a protonated form of the free HL(3) ligand, has been determined by a single crystal X-ray analysis. The geometry optimisation and infrared frequencies calculations of HL1, HL2, and H2L3+ and H2L4+ were performed using density-functional theory (DFT) calculations at the B3LYP/6-31G* level of the theory. The geometry of complex (1) was optimised at the same level of the theory.
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PMID:Synthetic, spectral, magnetic and in vitro cytotoxic activity studies of cobalt(II) complexes with cytokinin derivatives: X-ray structure of 6-(3-methoxybenzylamino)purinium chloride monohydrate. 1570 99

Fluorine compounds are widely used for the prevention of caries, and recently sodium fluorosilicate has been used in water fluorination. The cytotoxic effects of sodium fluorosilicate in several osteosarcoma and oral cancer cells were evaluated in this study by measurement of inhibition of cell proliferation. Human osteogenic sarcoma (HOS) cells were the most sensitive to sodium fluorosilicate treatment. Induction of apoptosis, such as nucleosomal DNA fragmentation and the appearance of apoptotic bodies, were observed in HOS cells by agarose gel electrophoresis and by flow cytometric analysis, respectively. The molecular mechanism of apoptosis induction in HOS was investigated by Western blot analysis. The level of Bcl-2 was decreased and consequent release of cytochrome c was increased. Caspase-3 was activated and the cleavage of poly (ADP-ribosyl) polymerase was increased. In conclusion, sodium fluorosilicate induces apoptosis in HOS cells through decrease in Bcl-2, the release of cytochrome c to the cytosol and activation of caspase-3.
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PMID:Induction of apoptosis by sodium fluorosilicate treatment in human osteogenic sarcoma (HOS) cells. 1581 63

We used positron emission tomography (PET) with [18F]fluoromisonidazole ([18F]FMISO) to study tumor hypoxia in six dogs with spontaneous sarcomas. The tumors were regarded as hypoxic if [18F]FMISO uptake exceeded normal tissue radioactivity by 40% (tumor/muscle ratio > 1.4) or if kinetic analysis indicated a positive [18F]FMISO tissue influx rate (Ki > 0) by a Patlak plot. Using these criteria, we found hypoxia in a fibrosarcoma grade II, an undifferentiated sarcoma, and an ostoeosarcoma, but not in a fibrosarcoma grade I, another osteosarcoma, and a myxosarcoma. In three animals, the tumor oxygen partial pressure (pO2) was also measured invasively using Eppendorf needle electrodes. In these cases, the Eppendorf measurements were confirmed by the [18F]FMISO PET results. In addition, [15O]H2O PET was performed in four dogs in order to assess tumor perfusion. Comparisons of the [18F]FMISO with [15O]H2O PET images in two cases showed that tumor hypoxia occurred in the tumor center with low perfusion, whereas perfusion was heterogeneous in a nonhypoxic tumor.
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PMID:Measurement of tumor hypoxia in spontaneous canine sarcomas. 1622 39

Poly(L-lactic acid)/hydroxyapatite hybrid nanofibrous scaffolds were prepared via electrospinning. The structure and morphology of the scaffolds were investigated using scanning electron microscopy, differential scanning calorimetry and Fourier transform infrared spectroscopy. The experimental results showed that the average diameter of hybrid nanofiber was similar to that of pure poly(L-lactic acid) fiber, but a new surface bonding (COO-) was formed in hybrid nanofiber which made the surface of the fiber coarse. The weight loss and water uptake of pure poly(L-lactic acid) scaffolds increased continuously and the viscosity-average molecular weight decreased in the phosphate buffer solution as time passed, while those of hybrid scaffolds were very much slowed down because the dissolving of hydroxyapatite particles acted as a physical barrier and blocked off the entry of water. The biocompatibility of the scaffold has been investigated by human osteosarcoma MG-63 cell culture on the scaffold. The preliminary results showed that cells were well adhered and proliferated better on the hybrid scaffolds than pure scaffolds.
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PMID:Poly(L-lactic acid)/hydroxyapatite hybrid nanofibrous scaffolds prepared by electrospinning. 1727 55

The oxovanadium(IV) complex of oxodiacetic acid (H2oda) of stoichiometry [VO(oda)(H2O)2], which presents an unprecedented tridentate OOO coordination, was thoroughly characterized by infrared, Raman, electronic, and electron paramagnetic resonance spectroscopies. The biological activity of the complex on the cell proliferation and differentiation was tested on osteoblast-like cells (MC3T3E1 osteoblastic mouse calvaria-derived cells and UMR106 rat osteosarcoma-derived cells) in culture. The complex caused inhibition of cellular proliferation in both osteoblast-like cells in culture, but the cytotoxicity was stronger in the normal (MC3T3E1) than in the tumoral (UMR106) osteoblasts. The effect of the complex in cell differentiation was tested through the specific activity of alkaline phosphatase of the UMR106 cells because they expressed a high activity of this enzyme. What occurs with other vanadium compounds [VO(oda)(H2O)2] is an inhibitory agent of osteoblast differentiation.
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PMID:Spectroscopic characterization of a VO2+ complex of oxodiacetic acid and its bioactivity on osteoblast-like cells in culture. 1787 58

Aluminium (Al) has been investigated as a neurotoxic substance. Al ranks among the potential environmental risk factors for Alzheimer's disease (AD). Epidemiological studies tested the relationship between Al in drinking water and AD, showing a significant correlation between elevated levels of monomeric Al in water and AD, although data to date remain inconclusive with respect to total Al. The aim of this study was to test whether or not Al exacerbates cellular toxicity mediated by the amyloid beta (Abeta) peptide. We evaluated the role of Al in modulating programmed cell death (apoptosis) in human cell cultures. We used the osteosarcoma cell line monolayer (SaOs-2) to demonstrate that treatment of SaOs-2 cultures with the Abeta peptide mid-fragment (25 to 35) at nano M, followed by co-incubation with physiological concentrations of aluminium chloride, which release monomeric Al in solution, led to marked expression of caspase 3, but not caspase 9, key markers of the apoptotic process. The same experimental conditions were shown to blunt significantly the proliferative response of normal human peripheral blood mononuclear cells (PBMC) to phytohemagglutinin (PHA) stimulation. Our observations support the hypothesis that Al significantly impairs certain cellular immune responses, and confirm that Al-mediated cell toxicity may play an important role in AD.
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PMID:Aluminium blunts the proliferative response and increases apoptosis of cultured human cells: putative relationship to Alzheimer's disease. 1808 47

Biodegradable and biocompatible polymeric scaffolds have been recently introduced for tissue regeneration purpose. In the present study we aimed to develop polymeric-based scaffolds for bone regeneration. Two polyesters, poly-beta-propiolactone (PBPL), poly-epsilon-caprolactone (PCPL) and two polyfumarates, polydiisopropyl fumarate (PDIPF), polydicyclohexyl fumarate (PDCF) were chosen to prepare films which can support osteoblastic growth. Scanning electron microscopy and water contact angle were used to characterize the matrices. Biodegradation studies were performed both in PBS buffer and using an in vitro macrophage degradation assay. Mouse calvaria-derived MC3T3E1 cells and UMR106 rat osteosarcoma cell lines were used to perform biocompatibility and cytotoxicity studies. The polyesters, the most hydrophilic polymers studied, showed a rougher and more porous surfaces than the polyfumarates. Under acellular conditions, only PBPL was degraded by hydrolytic mechanisms. However, macrophages performed an active degradation of all polymeric films. Osteoblasts developed well-defined actin fibres without evidence of cytotoxicity when growing on the films. The number of UMR106 osteoblasts that adhered to the PBPL-based film was higher than that of the cells attached to the PECL and polyfumarates (PDIPF and PDCF) matrices. Both UMR106 and MC3T3E1 osteoblastic lines showed protein levels comparable to control conditions, demonstrating that they grew well on all surfaces. However, UMR106 cells showed a significant increase in proliferation on polyester-derived scaffolds (PBPL and PECL). The alkaline phosphatase activity of UMR106, an osteoblastic marker, was significantly higher than that of control plastic dishes. MC3T3E1 cells expressed similar levels of this differentiation marker in all polymeric matrices. We found similar collagen protein content after 48 h culture of UMR106 cells on all surfaces. However, important differences were evident in the MC3T3E1 line. In conclusion, the synthetic polymeric-based scaffold we have developed and studied supports adhesion, growth and differentiation of two osteoblastic cell lines, suggesting that they could be useful in bone tissue regeneration.
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PMID:Biocompatibility and biodegradation of polyester and polyfumarate based-scaffolds for bone tissue engineering. 1827 18


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