Factors influencing the detachment of a polymer-associated Acinetobacter sp. from stainless steel

The role of an extracellular polymer secreted by an Acinetobacter sp. attached to stainless steel was investigated. Parameters expected to influence polymer conformation, viz. temperature, pH, ionic strength and the concentration of calcium and magnesium ions, were altered and the resulting detached bacteria enumerated. Increasing both the temperature and pH resulted in increased numbers of bacteria detached. The effects of increasing the concentration of sodium chloride up to 100 mM and magnesium or calcium chloride up to 30 mM were small and, although statistically significant, were considered unlikely to have had major influence on the association of the bacteria with the stainless steel surfaces. Treatments including ultraviolet irradiation of surface-associated bacteria always resulted in removal of greater numbers of bacteria when compared to treatments where irradiation was not employed. The results indicate that an adhesive extracellular acidic polysaccharide may mediate the attachment of the Acinetobacter sp. to stainless steel.     

Direct “Quantimet”-electron microscope linkage for the assessment of particle size distribution of polymer latices

Initial experiments using “Quantimet” image analysing computers linked directly with an electron microscope for the automated assessment of particle size and distribution in the sub-micron range are described. The ability to analyse polymer dispersions quickly and without the need for photographic procedures has been demonstrated. It has also been shown that statistical parameters of these dispersions can now be determined with a reasonable degree of certainty and with considerably less experimental difficulty Results obtained by this method have been compared with data obtained using micrographs assessed either manually or using the Zeiss-Endter instrument. Present limitations and future possibilities are indicated.     

DIFFERENTIATION OF YEASTS BY ELECTROPHORETIC METHODS

An examination of the esterase isoenzymes reacting with α-naphthyl acetate indicated five types of electrophoretic pattern in 94 strains of 54 species of 15 yeast genera. Groups classified according to esterase patterns agreed with accepted taxonomic groups, but there were no differences of obvious value for routine identification of separate species of yeasts. Strictly aerobic yeasts produced up to four bands of esterase activity; facultative anaerobes produced two lines or only one. Proteins detected by staining with trifalgic acid after electrophoresis formed identical patterns from all yeasts tested.     

Mechanisms of Breakaway Oxidation and Application to a Chromia-Forming Steel

Breakaway oxidation or chemical failure has beendescribed in this paper in terms of two possiblemechanisms and applied to the behavior of achromia-forming 20Cr-25Ni austenitic steel. Bothmechanisms relate to the depletion of chromium arisingfrom its selective oxidation and quantitative modelingof the depletion profile is used to identify thedominant chemical-failure mechanism as a function oftemperature. Intrinsic Chemical Failure (InCF) develops whenthe chromium concentration within the alloy at theoxide-metal interface is less than that in equilibriumwith chromia. This occurs at high temperatures, typically above 1390 K, but the temperature atwhich the alloy becomes susceptible to this form offailure increases as the alloy grain size decreases. Atlower temperatures, chemical failure is associated with the general depletion of chromium acrossthe specimen section to a level below which reformationof a healing chromia layer will not occur, should thesurface layer become damaged. In this regime, failure is termed Mechanically Induced ChemicalFailure (MICF).     

Ornithine decarboxylase over-expression stimulates mitogen-activated protein kinase and anchorage-independent growth of human breast epithelial cells

Inactivation of one X chromosome (X inactivation) in female mammals results in dosage compensation of X-chromosomally encoded genes between sexes. In the embryo proper of most mammals X inactivation is thought to occur at random with respect to the parental origin of the X chromosome. We determined on the cellular level the expression of the X-chromosomally encoded protein dystrophin in skeletal and cardiac muscle of female mice heterozygous for a null mutation of the dystrophin gene (mdx/+). In all muscles investigated (cardiac, anterior venter of digastric muscle, biceps brachii and tibialis anterior muscle) we found a mosaic expression of dystrophin-expressing versus non-expressing cells and determined their proportion with respect to the parental origin of the X chromosome. In all groups of mdx/+ mice the level and pattern of dystrophin expression were found to be dependent on the parental origin of the mdx mutation. Additionally, the extent of dystrophin expression was clearly dependent on the mouse strains (C57BL/10 and BALB/c) used to produce heterozygous mdx/+ mice. Variable differences and patterns of dystrophin expression in skeletal versus cardiac muscle were found that were strictly dependent on the parental source of the mdx mutation and the strain used to breed mdx/+ mice. Moreover, dystrophin expression was found to be different between the right side and the left side of the body in individual muscles, and this difference was clearly dependent on the parental origin of the X chromosome. Our data provide evidence that in the mouse embryo proper there is a non-random distribution of cells showing inactivation of the paternal versus the maternal X chromosome in skeletal and cardiac muscle, indicating a non-random X-inactivation. Besides gametic imprinting, strain-, tissue and position-dependent factors also appear to bias X inactivation.     

The polarized light microscopic appearance of caries-like lesions adjacent to restored cavities in the crowns and roots of extracted human teeth

Longitudinal clinical studies indicate consistently that secondary caries is the major cause of failure of restorations. Recently there has been an increase in the number of fluoride-containing materials coming to the market place and this has renewed the debate about the cariostatic effectiveness of such materials. The present study examined the histologic appearance of caries-like lesions adjacent to a non-fluoride-containing material (amalgam), a low fluoride-containing material (composite) and a moderate fluoride-containing material (glass-ionomer). The artificial caries system used to produce lesions has been previously reported and is a microbial system using Streptococcus mutans NCTC 10832. The lesions produced were similar to naturally occurring lesions in many respects, indicating the usefulness of this in vitro technique. Variations in the appearance of lesions were found adjacent to the different materials and the effect of the fluoride contained within two of the materials is discussed.     

Mice deficient for the secreted glycoprotein SPARC/osteonectin/BM40 develop normally but show severe age-onset cataract formation and disruption of the lens

SPARC (secreted protein acidic and rich in cysteine, also known as osteonectin/BM40) is a secreted Ca2+-binding glycoprotein that interacts with a range of extracellular matrix molecules, including collagen IV. It is widely expressed during embryogenesis, and in vitro studies have suggested roles in the regulation of cell adhesion and proliferation, and in the modulation of cytokine activity. In order to analyse the function of this protein in vivo, the endogenous Sparc locus was disrupted by homologous recombination in murine embryonic stem cells. SPARC-deficient mice (Sparctm1Cam) appear normal and fertile until around 6 months of age, when they develop severe eye pathology characterized by cataract formation and rupture of the lens capsule. The first sign of lens pathology occurs in the equatorial bow region where vacuoles gradually form within differentiating epithelial cells and fibre cells. The lens capsule, however, shows no qualitative changes in the major basal lamina proteins laminin, collagen IV, perlecan or entactin. These mice are an excellent resource for further studies on how SPARC affects cell behaviour in vivo.