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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this in vitro study we investigated the influence of ionizing gamma rays on the stability in the region of the dentinoenamel junction. We removed the enamel on the labial surface of 30 incisors of bovines up to the dentinoenamel junction, so that a circular area of enamel with a diameter of 2.0 +/- 0.1 mm was left and an enamel cylinder was created. 15 teeth were irradiated by a cobalt-60-source (energy dose 70 Gy). The other 15 teeth were used as controls. Using a material testing apparatus the shear bond strengths were measured by breaking off the enamel cylinders. Furthermore, the breaking modes were investigated in SEM. Comparing the results of the shear bond strength experiments, it was obvious that the stability in the region of the dentinoenamel junction was significantly less among the irradiated teeth than among the non-irradiated teeth. The median value of the gamma ray treated teeth was x = 19.1 MPa and that of the non-ray-treated teeth was x = 37.4 MPa. The non-irradiated teeth showed fractured surfaces only in dentin in 10 cases and in 5 cases in both dentin and enamel. In contrast to that, the irradiated teeth had fractured surfaces in 12 cases exclusively in dentin and only in 3 cases the enamel was also fractured. These results lead us to conclude that changes of biophysical property of teeth can be caused by the influence of ionizing rays.
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PMID:An experimental study of the stability of irradiated teeth in the region of the dentinoenamel junction. 130 87

The effect of biomaterials on the activation of human neutrophils was studied. Human neutrophils were incubated with F-75 cobalt-based alloy or polystyrene microspheres of a nonphagocytosable size with two times total neutrophil plane surface area. Scanning and transmission electron microscope (SEM, TEM), energy dispersive x-ray microanalysis (EDX), and graphite furnace atomic absorption spectroscopy (GFAAS) were used to analyze changes in cellular morphology and metal content. This report presents evidence that human PMNs display morphological changes related to foreign material challenge, including activation on F-75 bead surfaces, pinocytosis of corrosion products, formation of intracellular vacuoles, degranulation, etc. Moreover, when PMNs were present, the corrosion release rate of F-75 increased as much as three times over cell-free controls.
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PMID:Human neutrophil response to short-term exposure to F-75 cobalt-based alloy. 142 68

1. The neurons of the retina have electrical properties that are different from those of most of the other neurons of the central nervous system. To identify the voltage-gated ion channels found in the retina, we screened mouse retinal cDNA libraries with oligonucleotide probes homologous to the mammalian K+ channel MBK1 (Kv1.1) and ligated two partial clones to produce a full-length clone with no significant differences from MBK1. 2. Expression of MBK1 mRNA was determined by RNAse protection. MBK1 mRNA was detected in retinal RNA and was also detected in brain, liver, and heart RNAs. 3. We transcribed the full-length clone, injected it into oocytes of Xenopus laevis, and measured the membrane currents 2 to 6 days later. Depolarization from a holding voltage of -90mV induced a slowly activated outward current with a peak value as large as 20 microA. The current inactivated very slowly with a single exponential time course [mean time constant, 6.5 +/- 0.4 sec (SEM) for activation voltage of -10mV]. 4. The outward current was reduced to half-maximal by 0.42 mM tetraethylammonium, 1.1 mM 4-aminopyridine, and 3.2 mM Ba2+ but was not significantly attenuated by Co2+ (1 mM). 5. The reversal potential (measured with tail currents) changed by 53mV per decade change of [K+] from 1 to 77 mM. 6. The voltage for half-maximal activation of the conductance was -26.6mV (+/- 1.7mV), and the voltage required for an e-fold increase in conductance was 6.9mV (+/- 0.5mV). 7. Thus, the mRNA for MBK1 found in the mouse retina causes the expression of a voltage-dependent K+ current which has properties suitable for may retinal neurons.
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PMID:The potassium channel MBK1 (Kv1.1) is expressed in the mouse retina. 172 58

Different studies have shown that various substances may have an influence on early human dental plaque formation. The purpose of the present study was to compare on tooth substances and supporting prosthetic materials the amount of plaque deposition by SEM and the quantity of selected bacteria using anaerobic culturing techniques. 5 bridges, replacing a missing molar or premolar, were incorporated in 3 patients. In the midbuccal area of each pontic, a semi-precision attachment was placed allowing the insertion of the following test facings: enamel, dentine, non gamma 2-amalgam, alloys of 85% and 55% gold, silver-palladium, chrome-cobalt, chrome-cobalt-titanium, and ceramic. For each material, 2 facings were fabricated. After 4 and 24 hours in situ, bacteriological samples were taken and processed for further identification. After a 2nd period of 4 and 24 hours in situ, the same facings were carefully removed and prepared for SEM-examination. All 4-hour specimens exhibited various areas covered by plaque, the amount of which varied with the different supporting substances. The very smooth surfaces (e.g., gold) harbored sparse deposits, while the rougher (e.g., amalgam) were covered by more plaque. After 24 hours of plaque development, an increase in the number of micro-organisms was noted for all the specimens. After 4 and 24 hours of plaque accumulation, no specific trends suggesting a preferential colonization on the different substances were observed. This study has shown that the amount of early deposits on different substances seems to be related to the degree of their surface roughness, while plaque formation was qualitatively similar.
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PMID:In vivo early human dental plaque formation on different supporting substances. A scanning electron microscopic and bacteriological study. 180 21

Twenty-five squamous cell carcinoma (SCC) cell lines from 20 patients with head and neck cancer were assessed for radiosensitivity in vitro using a 96-well plate assay. Four non-SCC lines were also tested. Radiation sensitivity of individual cell lines was compared using the area under the survival curve (AUC) as a measure of the mean inactivation dose. Tumor lines were tested with either a cobalt-60 (60Co) gamma-irradiator having a dose rate of 100 cGy/minute or with a 4-meV photon beam having a dose rate of 200 cGy/minute. The mean AUC of the 25 SCC cell lines was 188 +/- 7 (SEM) cGy (range, 100 to 250 cGy) whereas the four non-SCC lines had a mean AUC of 225 +/- 9 cGy. The SCC cell lines with mean inactivation dose values greater than 188 cGy were classified as relatively radioresistant whereas those with values less than 188 cGy were considered relatively radiosensitive. In seven cases SCC cell lines were derived from patients who had already received radiation therapy. In four of these cases the tumor cell lines were radioresistant (AUC, 210 to 250) but in the other three cases the tumor lines were radiosensitive (AUC, 160 to 180). Thus, failure of a tumor to respond to radiation did not always select for radioresistant cells. The mean of the AUC for cell lines from previously irradiated patients (197 +/- 11 cGy) did not differ significantly from that of the cell lines from patients who received no prior radiation therapy (182 +/- 9 cGy). However, among radiation-resistant lines those from the four previously irradiated patients were significantly more resistant (mean AUC = 235 +/- 9) than seven other radioresistant lines from nonirradiated patients (mean AUC, 208 +/- 4) (P = 0.0194). In four cases more than one cell line was derived from different tumor specimens in the same patient. In each of these cases the lines from the same patients were similar to one another in their degree of radioresistance. Based on these observations the authors conclude that the degree of in vitro radiation resistance is an inherent property of some squamous cell tumors.
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PMID:In vitro radiation resistance among cell lines established from patients with squamous cell carcinoma of the head and neck. 202 37

Among other characteristics, the steady-state current-voltage relationship of patch-clamped single atrial myocytes from guinea-pig hearts is defined by an outward current hump in the potential region -15 to +40 mV. This hump was reversibly suppressed by Co2+ (3 mM) or nitrendipine (5 microM) and enhanced by Bay K 8644 (5 microM). The maintained outward current component suppressed by Co2+ extended between -15.2 +/- 1.9 mV and +39.5 +/- 1.7 mV (mean +/- SEM of 14 cells) and has an amplitude of 95.7 +/- 9.4 pA at +10 mV. In isochronal I-V curves, the hump was already visible at 400 ms with essentially the same amplitude as at 1500 ms. The Co2+-sensitive outward current underlying the hump was poorly time-dependent during 1.5 s voltage pulses but slowly relaxed upon repolarization. Tail currents reversed near the K+ equilibrium potential under our experimental conditions. The current hump of the steady-state I-V curve was also abolished by caffeine (10 mM) or ryanodine (3 microM), both drugs that interfere with sarcoplasmic reticulum function. Apamin (1 microM) or quinine (100 microM) but not TEA (5-50 mM) markedly reduced its amplitude. However, at similar concentrations as required to inhibit the hump, both apamin and quinine appeared to be poorly specific for Ca2+-activated K+ currents in heart cells since they also inhibited the L-Type Ca2+ current. It is concluded that a long lasting Ca2+-activated outward current, probably mainly carried by K+ ions but not sensitive to TEA, exists in atrial myocytes which is responsible for the current hump of the background I-V curve.
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PMID:A long lasting Ca2+-activated outward current in guinea-pig atrial myocytes. 248 61

We have characterized specific receptors for tetradecapeptide somatostatin (SS-14) of rat brain using 125I-labeled Tyr11-SS-14([125I-Tyr11]SS-14) as radioligand. [125I-Tyr11]SS-14 binding was sensitive to time, pH, temperature and ionic strength of the buffer, and was optimal in 50mM HEPES/KOH buffer, pH 7.5, at 25 degrees C for 60 minutes. Scatchard analysis indicated that the rat forebrain membranes had a single binding site with an apparent dissociation constant (Kd) of 0.522 +/- 0.044 nM and maximum binding capacity (Bmax) was 233 +/- 37 fmol/mg protein (mean +/- SEM). Ca2+, Mg2+, Mn2+ and Co2+ had a significant effect on the specific binding, which indicates that these metal ions might affect somatostatin receptor activity in the brain. Among CNS acting drugs, Ca2+ antagonists, antischizophrenic drugs, antidepressants and anticholinergic drugs had relative effects on [125I-Tyr11]SS-14 bindings to rat cerebral cortex membranes.
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PMID:Biochemical and pharmacological characterization of somatostatin receptors in rat brain. 257 1

An improved holder has been designed for a cobalt calibrating standard used in an EDS Link 10,000 system attached to a JEOL 840 SEM. This holder allows the calibration of the EDS software for a wide range of samples differing in size, surface and height. These differences usually cause difficulties during quantitative analyses. The new holder allows the position of the cobalt to be adjusted according to the size and height of the sample.
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PMID:A new versatile holder for the calibrating standard used for quantitative analysis in a JEOL 840 SEM. 274 Aug 58

Currents were generated by depolarizing pulses in voltage-clamped, dissociated neurons from the CA1 region of adult guinea pig hippocampus in solutions containing 1 microm tetrodotoxin. When the extracellular potassium concentration was 100 mM, the currents reversed at -8.1 +/- 1.6 mV (n = 5), close to the calculated potassium equilibrium potential of -7 mV. The currents were depressed by 30 mM tetraethylammonium in the extracellular solution but were unaffected by 4-aminopyridine at concentrations of 0.5 or 1 mM. It was concluded that the currents were depolarization-activated potassium currents. Instantaneous current-voltage curves were nonlinear but could be fitted by a Goldman-Hodgkin-Katz equation with PNa/PK = 0.04. Conductance-voltage curves could be described by a Boltzmann-type equation: the average maximum conductance was 65.2 +/- 15.7 nS (n = 9) and the potential at which gK was half-maximal was -4.8 +/- 3.9 mV (mean +/- 1 SEM, n = 10). The relationship between the null potential and the extracellular potassium concentration was nonlinear and could be fitted by a Goldman-Hodgkin-Katz equation with PNa/PK = 0.04. The rising phase of potassium currents and the decay of tail currents could be fitted with exponentials with single time constants that varied with membrane potential. Potassium currents inactivated to a steady level with a time constant of approximately 450 ms that did not vary with potential. The currents were depressed by substituting cobalt or cadmium for extracellular calcium but similar effects were not obtained by substituting magnesium for calcium.
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PMID:Potassium current activated by depolarization of dissociated neurons from adult guinea pig hippocampus. 284 59

The role of calcium ion mobilization in modulation of secretion of the ovarian protein hormone relaxin by porcine luteal cells was examined by use of a reverse hemolytic plaque assay. In this assay, luteal cells were cocultured in monolayers with protein-A-coupled ovine erythrocytes. In the presence of porcine relaxin antiserum and complement, a zone of hemolysis, a plaque, developed around relaxin-releasing luteal cells. The rate of development of plaques in time-course experiments was used in this study as an index of the rate of relaxin release. Exposure of luteal cell-containing monolayers to the calcium-mobilizing agent A23187 (40 nM to 5 microM) resulted in a dose-related increase in the rate of relaxin-plaque formation. This effect [and the influence of a stimulatory secretagogue, prostaglandin E2 (PGE2; 1 microM)] was suppressed by coculture with Co2+ (5 mM), a calcium channel blocker. These results are consistent with the view that calcium ion redistribution within porcine luteal cells forms a pathway that subserves, at least in part, the rates of basal and stimulated relaxin release in vitro. However, A23187 was equally effective in enhancing the rate of plaque formation when the monolayers were bathed in a low calcium medium (mean +/- SEM, 6.61 +/- 0.92 microM Ca2+), rather than a calcium-replete medium (1.56 +/- 0.09 mM Ca2+). Likewise, neither basal nor PGE2-stimulated (1 microM) relaxin secretion was abrogated by culture of monolayers in low calcium medium. These data suggest that the stimulatory effect of A23187 (and perhaps PGE2) arose predominantly through redistribution of calcium stored within intracellular sites in luteal cells, rather than entrance of calcium into the cell from the extracellular medium. Yet, incompatible with this interpretation, we observed that TMB-8 [8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride; a putative inhibitor of intracellular calcium redistribution] enhanced rather than blocked A23187- or PGE2-stimulated relaxin release. This result is consistent with the possibility that TMB-8 mobilized (rather than blocked) calcium in this cell system or that it acted via calcium-independent mechanisms. We conclude that calcium mobilization has the potential to act as a molecular pathway that transduces secretion of an ovarian peptide hormone, relaxin. However, the exact nature and physiological role(s) of the Ca2+ pathway in the control of relaxin secretion and the interrelationships of this mechanism with other intracellular messengers that may also modulate ovarian peptide secretion remain to be more clearly defined.
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PMID:Regulation of relaxin release from monodispersed porcine luteal cells: effect of calcium ionophore A23187 and calcium channel blockers. 313 4


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