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Biomedical subjects

J Arends

Publications and source records attributed to J Arends.

At least 181 records · Page 10Linked to original sources
PubMed1986

Kinetics of adhesion of the oral bacterium Streptococcus sanguis CH3 to polymers with different surface free energies.

The kinetics of adhesion of Streptococcus sanguis CH3 from suspension to polymers with different surface free energies were studied by using three bacterial concentrations (2.5 X 10(7), 2.5 X 10(8), and 2.5 X 10(9) cells per ml-1). Substratum surface free energies (gamma s) ranged from 18 to 120 erg cm-2. The kinetics of bacterial adhesion to these surfaces showed a typical two-step adhesion process, indicating an equilibrium in both steps. In the initial adhesion step (step 1), low equilibrium numbers of adhering bacteria were counted on substrata with surface free energies lower than 55 erg cm-2. A maximal number adhered on substrata with higher surface free energies. At the lowest bacterial concentration tested, the highest number of bacteria were found on substrata with a surface free energy around 55 erg cm-2. For each substratum, step 2 started after a characteristic time interval tau, being short (30 min) for gamma s less than 50 and long (120 min) for gamma s greater than 50 erg cm-2. The relationship between the substratum surface free energy and the number of bacteria adhering at equilibrium after step 2 was similar to, although less distinct than, that during step 1 with a slight indication of a bioadhesive minimum around gamma s = 35 erg cm-2. The results are indicative of a two-step adhesion model, in which step 1 is controlled by macroscopic substratum properties.

Adhesiveness↗
PubMed1986

The nature of early caries lesions in enamel.

Since 1935, various mechanisms have been suggested for the formation of subsurface lesions and, in particular, the surface layer covering enamel lesions. The relatively intact mineral-rich and porous surface layer is most likely caused by kinetic events. The suggested mineral-rich outer layer in sound enamel, the organic matrix, the pellicle, or a non-uniform ion distribution have all been shown to be non-essential for surface layer formation; they may, however, influence the rate of surface layer formation. Models based on outer surface protection by adsorbed agents, the dissolution-precipitation mechanism, and combinations of these two models, as well as models based on porosity or solubility gradients, are discussed in this paper together with their advantages and disadvantages. Most models have not explained some important recent experimental observations on initial in vivo caries lesion formation: e.g., initial enamel lesions formed in vivo do not have a surface layer initially but develop this mineral-rich layer later on; and the fact that the F- level in the solid sound enamel is not determining the subsurface lesion formation. Furthermore, the observations that in vitro fluoride ions in the liquid at very low levels (approximately equal to 0.02 ppm) determine surface layer formation are difficult to explain. A new kinetic model for subsurface lesion formation is described, in which inhibitors such as F- or proteins play an important role. The model predicts that if lesions depth and demineralization period are denoted by df and t, lesion progress can be described by: dfp = alpha t + c, where alpha and c are constants with 1 less than or equal to p less than or equal to 3, depending on the lesion formation conditions. If lesion progress is entirely diffusion-controlled, p = 3, corresponding to low inhibitor concentrations; if the inhibitor content is so high that the progress is controlled by processes at the crystallite surface, p = 1. A kinetic mechanism for surface layer formation in vivo is proposed, based on the assumption that F- is a main inhibitor in the plaque-covered acidic in vivo situation. The inhibiting fluoride, adsorbed onto the crystallite surfaces at OH- vacancies, originates from the so-called fluoride in the liquid phase (FL) between the enamel crystallites. Under acidic conditions (plaque), we have, due to an influx of fluoride from the saliva or plaque as FL, an aqueous phase in the enamel supersaturated with respect to the mineral for a small distance (x*) only.(ABSTRACT TRUNCATED AT 400 WORDS)

Absorption↗
PubMed1986

Micro-Raman line broadening in synthetic carbonated hydroxyapatite.

Using a Raman microspectrometer, we have recorded Raman spectra of synthetically produced hydroxyapatite samples with varying carbonate contents. The apatites were produced from aqueous solutions at about 40 degrees C. From line-broadening values of the symmetric phosphate stretch, it was concluded that the carbonate substitution in these lattices has a maximum of 4.5 wt %. Both phosphate and hydroxyl ions seem to be involved in the carbonate substitution process.

Carbonates↗
PubMed1986

Wetting properties of human saliva and saliva substitutes.

Contact angle measurements were employed so that we could study the wetting properties of human whole saliva and saliva substitutes containing mucins or carboxymethylcellulose (CMC) on human oral mucosa (in vivo) and on ground and polished human enamel (in vitro). A new approach was introduced for measuring contact angles on human oral mucosa in vivo. It was shown that the wetting properties of CMC- and mucin-containing saliva substitutes on human enamel were significantly better than those of human whole saliva. On human oral mucosa, the wetting properties of CMC-containing saliva substitutes and human whole saliva were comparable, but were surpassed by those of the mucin-containing saliva substitutes. Mucin-containing substitutes thus provide good wetting properties on ground and polished enamel as well as on oral mucosa.

Aged↗
PubMed1986

The inhibition of demineralization of human enamel after fluoride varnish application as a function of the fluoride content. An in vitro study under constant composition demineralizing conditions.

The inhibiting effect of a 24 hours application of a fluoridated varnish with various fluoride contents on demineralization of human sound enamel was evaluated in vitro. The varnishes used had the same polyurethane base (Fluor Protector) and contained 0.7; 0.1; 0.05 and 0 wt% fluoride, resp. A constant composition technique was used to demineralize varnished and non-varnished specimens at a pH of 5 for periods upto 2 weeks. Microhardness measurements were carried out after several time intervals to follow mineral loss in time longitudinally. At the end of each experimental run microradiography was carried out to investigate 1) lesion type, 2) lesion depth and 3) mineral loss. It is shown in this study that the fluoride releasing varnishes applied on the enamel for 24 hours can inhibit demineralization completely. No demineralization inhibition with the 0% fluoride varnish application was observed.

Decalcification Technique↗
PubMed1986

Immunofluorometry of thyrotropin, from whole-blood spots on filter paper, to screen for congenital hypothyroidism.

We have evaluated a time-resolved immunofluorometric assay (IFMA) for determining thyrotropin. This "sandwich"-type system involves two monoclonal antibodies directed against different epitopes. A linear relationship between signal and thyrotropin concentration was observed up to 6000 milli-int. units/L. This procedure takes one day, vs six days with our present RIA technique, and requires only a tenth as much sample. Furthermore, intra- and interassay CVs are lower than with RIA. Assay of 19 paper-disc blood specimens from newborns identified as having congenital hypothyroidism, both by RIA and by clinical evidence, also gave positive results with IFMA. In prospective assay of 3944 specimens by both methods we identified one case of congenital hypothyroidism, which was detected by both techniques. Technical false-positive reactions, identified as such by repeated analyses, were fewer with the IFMA method than with RIA.

Antibodies, Monoclonal↗
PubMed1985

[Hypoglycemia with loss of consciousness during insulin therapy as an initial symptom of Addison's disease. Report of 2 cases].

Within a six-month period, two type-I diabetics were admitted because of labile metabolic state with recurrent severe hypoglycaemia and unconsciousness. In both patients electrolytes were normal on admission. There were at first only few pointers to Addison's disease. But in both primary adrenocortical insufficiency was demonstrated to be the cause of the symptoms. Serological tests suggested an autoimmune genesis. Recurrent severe hypoglycaemia and unconsciousness in insulin-treated diabetics indicates that adrenocortical insufficiency should be excluded.

Addison Disease↗