Sol-gel synthesis, structure and bioactivity of polycaprolactone/CaO . SiO2 hybrid material.

A method has been developed to cast novel organic/inorganic polymer hybrids from multicomponent solutions containing tetramethyl orthosilicate, calcium nitrate tetrahydrate, polycaprolactone, water, and methylethyketone via sol-gel process. The existence of the hydrogen bonds between organic and inorganic components of the hybrid and hydroxyapatite formation on the surface was proved by Fourier transform infrared analysis. The morphology of the hybrid material was studied by scanning electron microscopy. The structure of a molecular level dispersion was disclosed by atomic force microscopy, pore size distribution, and surface measurements. The infrared spectra of the hybrid relative to sample soaked in a fluid simulating the composition of human blood plasma suggests that polycaprolactone/CaO * SiO(2) hybrid material synthesised via sol-gel process is bioactive as well as the CaO * SiO(2) gel glass.

Effect of the substitution of Y2O3 for CaO on the bioactivity of 2.5CaO.2SiO2 glass.

Glasses were prepared whose composition is defined by the following general formula: (2.5-x)CaO.x/3Y2O3.2SiO2 (0 < or = x < or = 1). Their behaviour when they were soaked in a simulated body fluid (SBF) and their thermal properties (glass transformation and softening temperatures, Tg and Ts respectively) were studied Tg and Ts increase with the Y2O3 content. The trend can be explained on the basis of the increased structural rigidity when Ca2+ ions are substituted by Y2+ ions, because of the formation of stronger bonds to the oxygen. The bioactivity was studied by means of electron microscopy equipped with an energy dispersive system for elemental analysis and IR spectroscopy. All the glasses studied except the one with the greatest amount of Y2O3. x = 1.0, reacted with SBF by forming a calcium phosphate layer. The experimental results suggest that the bioactivity is negatively influenced by the Y2O3 content: the tendency to form a calcium phosphate layer is reduced the greater the amount of CaO substituted. A comparison with literature data indicates that the amount of Y2O3 that can be substituted depends on the CaO content of the base CaO-SiO2 glass. The experimental results are in good agreement with the mechanism reported in the literature. After 7 days soaking, crystalline hydroxyapatite is formed in the Y2O3-free glass and in the glasses of low Y2O3 content (x-0.2).

Bioactivity of 1.25CaO.SiO2 glass: an FTIR and X-ray study on powdered samples.

Powdered samples (170-230 mesh) of a glass of composition 1.25CaO.SiO2 were soaked in a simulated body fluid (SBF). The powders were submitted to Fourier transform infrared transmission spectroscopy as coarse powders (such as drawn out from the SBF) and as fine powders (soaked and subsequently ground). Soaked samples were submitted to differential thermal analysis (DTA) and the crystalline phases formed during heating in the DTA apparatus were identified by means of X-ray diffraction analysis. The method appears to be useful in studying the mechanism of deposition of the hydroxyapatite layer. It is documented, by using the same method, that the mechanism involves the reactions of hydrolysis and successive condensation and repolymerization of the silicate substrate. These reactions are very fast. Extensive Ca2+ cation depletion occurs, but appears to be slower.

Effect of the substitution of La2O3 for CaO on the bioactivity of 2.5CaO.2SiO2 glass.

Glasses of the following composition were prepared: (2.5-x)CaO.x/3La2O3.2SiO2 (0 < or = x < or = 1). Their behavior when soaked in a simulated body fluid (SBF) was studied by means of electron microscopy (EM) equipped with an energy-dispersive system (EDS) for elemental analysis, IR spectroscopy, and x-ray diffraction. All the studied glasses react with SBF by forming a calcium phosphate layer. This layer appears to be increasingly thinner with increasing amounts of La2O3 substituted. The experimental results are in good agreement with mechanisms reported in the literature. Moreover they suggest that lanthanum oxide is retained in the layer below the phosphate. After 6 days of soaking, crystalline hydroxyapatite is formed in the case of La2O3 free glass.

Apatite formation on (2-x)CaO.x/3 M2O3 x 2SiO2 glasses (M = La, Y; 0 < or = x < or = 0.6) in a simulated body fluid.

Glasses were prepared by substituting La2O3 or Y2O3 for CaO in glassy wollastonite composition (CaO.SiO2). Their behaviour when they are soaked in a simulated body fluid (SBF) was studied by means of an electron microscope equipped with an energy dispersive system for elemental analysis, and by means of IR spectroscopy. Electron microscopy and energy dispersive microanalysis were performed on samples soaked as polished bulk samples, and IR analysis was on samples soaked as fine powders. A carbonate-containing hydroxyapatite layer is formed when glasses of low La2O3 content are soaked in SBF. When Y2O3-containing glasses are considered, even in the case of small substitution for CaO, the same layer forms only on fracture surfaces. The experimental results agree with the mechanism reported in the literature.

The regulation of intracellular Mg2+ in guinea-pig heart, studied with Mg(2+)-selective microelectrodes and fluorochromes.

Because of the reported presence of a Na(+)-Mg2+ exchanger in guinea-pig but not in ferret myocardium, the Mg2+ extrusion mechanism in guinea-pig myocardium has been reinvestigated using Mg(2+)- and Na(+)- selective microelectrodes and the fluorochromes mag-fura-2 and -5. The mean [Mg2+]i measured with microelectrodes in trabeculae or papillary muscles was 0.72 mmol/l (n = 22, thirteen experiments; range 0.42-1.23 mmol/l). Increasing [Mg2+]o from 0.5 mmol/l to either 10.5 or 20 mmol/l caused small increases in [Mg2+]i. Decreasing [Na+]o by 50% had no effect on the [Mg2+]i and there was no change in [Na+]i on increasing [Mg2+]o from 0.5 to 10.5 mmol/l. Varying pHo or changing pHi with NH4Cl did not influence the [Mg2+]i. In vitro calibration of mag-fura-2 and -5 using the ratio method gave values for K'd (experimentally determined dissociation constant) of 22.2 +/- 2.7 (mean +/- S.D., n = 7) and 25.7 +/- 1.3 (n = 4) mmol/l respectively. Mag-fura-2 reacted to physiological concentrations of Ca2+ and mag-fura-5 to changes in pH. In isolated myocytes, Na+ removal gave an apparent increase of [Mg2+]i with mag-fura-2 but not with mag-fura-5. However, when the pHi was altered with NH4Cl mag-fura-5 showed an apparent decrease in [Mg2+]i on application and an apparent increase on removal, with a time course similar to the pHi changes. It is concluded that Mg2+ extrusion in guinea-pig myocardium is not via a Na(+)-Mg2+ exchanger. The use of mag-fura-2 and -5 are limited in their application because of Ca2+ and H+ sensitivity respectively.

Calcium buffer solutions and how to make them: a do it yourself guide.

In measurements of the intracellular free calcium concentration ([Ca2+]) using either microelectrodes or fluorescent probes, calibration is normally carried out in EGTA calcium buffer solutions. In the first part of the article the general properties of calcium buffer solutions are discussed, the equations used to calculate the apparent calcium binding constant (Kapp) are derived, and the difficulties in the calculation are discussed. The effects of the purity of EGTA as well as the influence of calcium contamination on the buffer solutions are explained. Because of the difficulties in calculating Kapp, and the importance of EGTA purity and calcium contamination, it is suggested that it is easier to measure all three under the appropriate experimental conditions using the method of Bers (1982). In the second part a do-it-yourself guide to the preparation of EGTA calcium buffer solutions is given. An experimental example is provided using the Bers method to measure purity, contamination, and Kapp. It is concluded that unless all three factors are known it is not possible to prepare accurate EGTA calcium buffer solutions.

Use of ion-sensitive microelectrodes to study intracellular free magnesium concentration and its regulation in mammalian cardiac muscle.

Ion-sensitive microelectrodes (ISEs) have been used to measure intracellular [Mg2+] ([Mg2+]i) in cardiac muscle, although most measurements have tended to overestimate the value due to the poor selectivity of the Mg2+ ionophore in the sarcoplasm and to inaccurate collation of individual ISE measurements. This paper highlights the correct method for analysis of data from multiple ISE experiments. Since [Mg2+]i is constrained at a lower concentration than would be expected by passive distribution of the ion, some of the possible mechanisms underlying Mg2+ extrusion from ferret ventricular myocardium were investigated. During elevation of the extracellular [Mg], mean [Mg2+]i rose from 1.61 to 1.91 mM. The same intervention had no significant effect on membrane potential, intracellular [Na+] or pH measured with ISEs, and there was no change in resting [Ca2+], as assessed from fura-2 fluorescence. The data are not consistent with a simple mechanism for Na(+)-Mg2+ exchange as the primary mode of Mg2+ regulation in cardiac muscle or with an Mg2+ extrusion mechanism involving steady-state ion exchange.

Intracellular free magnesium and its regulation, studied in isolated ferret ventricular muscle with ion-selective microelectrodes.

Intracellular free magnesium ([Mg2+]i) was measured in isolated ferret papillary muscles using ion-selective microelectrodes filled with the new magnesium sensor ETH 5214. This new sensor, unlike its predecessor ETH 1117, does not react to marked changes in K+, Na+ or pH. Reducing Ca2+ from 20 microM to around 10 nM also did not affect the response so these electrodes are ideally suited to study intracellular Mg2+ and its regulation. The mean value for the [Mg2+]i from thirty-two experiments (forty-two impalements) was 0.85 mM, confirming previous estimates from this laboratory. Intracellular Mg2+ is not passively distributed and the possibility that Mg2+ is transported out of the cell by a Na(+)-Mg2+ exchanger was investigated. An increase in [Mg2+]o caused an increase in [Mg2+]i, as did stepwise reduction in the [Na+]o. However, this increase in [Mg2+]i on Na+ reduction also occurred in Mg2(+)-free solution suggesting that the increase in [Mg2+]i was due to the increase in intracellular Ca2+ on Na+ reduction. Moreover, increasing [Na+]i by strophanthidin did not change the [Mg2+]i and on increasing [Mg2+]o there was no reduction in the [Na+]i. Blocking ATP production lead to small increases in the [Mg2+]i. These results are not consistent with a Na(+)-Mg2+ exchanger as being the main outward transport mechanism for Mg2+ in this tissue.

[Neurocysticercosis]. / Neurozystizerkose.

A report is presented on a 30-year-old Ecuadorian and a 40-year-old Sicilian with ventricular neurocysticercosis. The disease was manifested as occlusive hydrocephalus with signs of acute augmentation of intracranial pressure requiring emergency ventricular drainage. Subsequently several cysts were removed from the ventricles of both patients by craniotomy. One of the patients was discharged and left for Ecuador after operation while the other received antiparasitic therapy with praziquantel; this did not, however, contribute to an improvement of the symptoms. The diagnosis, differential diagnosis and therapy of neurocysticercosis are discussed.