Studies on the bacterial spore coat. 5. Effect of sodium dodecyl sulphate sonic treatment on the spore of Bacillus thiaminolyticus.
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Alanine↗
Biomedical subjects
K Watabe
Publications and source records attributed to K Watabe.
Effect of steam-heat treatment with/without divalent cations on the inactivation of lipopolysaccharides from several bacterial species.
The inactivation of endotoxin from six species of smooth gram-negative bacteria (S-form) by steam-heat treatment was investigated using the Limulus amebocyte lysate (LAL) assay. Biphasic decreases of endotoxins from four species of bacteria were observed upon steam-heat treatment of 1 microgram/ml endotoxin solution at 121 degrees C in a steam sterilizer. A lag time, however, was observed in the inactivation profiles of V. cholerae and P. aeruginosa. Distinct differences in heat resistance were observed among the bacterial species. The decrease rate was found to be concentration-dependent, and endotoxins at low concentrations (less than 10 ng/ml) were inactivated by the treatment to below the detection limit of the LAL assay. The time-course of the decrease of endotoxin from rough strains (R-form) resembled that of the respective S-form. The inactivation of R-form, especially Rc mutant, endotoxin was markedly affected by divalent cations such as Mg2+ and Ca2+, which appear to promote reaggregation of the endotoxin.
Calcium Chloride↗
Enhancing effect of non-ionic surfactant on the inactivation of lipopolysaccharide by steam-heat treatment I.
Polyoxyethylene (20) sorbitan mono-fatty acid esters strongly enhanced the inactivation of lipopolysaccharide (LPS) by steam-heat treatment at 121 degrees C, as assayed by using the Limulus amebocyte lysate (LAL) and the pyrogen test. In an aqueous solution containing 0.1% surfactant, the decrease of LPS (1 microgram/ml) from E. coli 055:B5 at 121 degrees C followed first-order kinetics. Based on the LAL assay, 0.1% surfactant was essential to achieve 3-log cycle reduction of LPS with concomitant loss of pyrogenicity by steam-heat treatment for 20 min at 121 degrees C. Steam-heat treatment for 20 min at 121 degrees C in the absence of surfactant was insufficient to achieve depyrogenation. Polyoxyethylene (9) lauryl ether and decaglycerin mono-laurate similarly enhanced depyrogenation by steam-heat treatment. The effects of all the surfactants were concentration-dependent for all of the six kinds of LPS examined.
Feasibility Studies↗
Enhancing effect of nonionic surfactant on the inactivation of lipopolysaccharide by steam-heat treatment II.
n-alkylpolyoxyethylene surfactants (CnH2n+1O(CH2CH2O)mH; CnEm) showed a strong enhancing effect on the inactivation of lipopolysaccharide (LPS) by heat treatment over a wide range of temperatures. The effect of CnE8 (n = 10-16) was observed above the critical micelle concentration (CMC) and above the cloud point, and was influenced by the length of the alkyl chains. The efficacy of the surfactants was in the order C10E8 < C12E8, C16E8 < C14E8. However, the hydrophilic moiety seemed to have no influence. An 80-95% solution of n-butanol showed a similar effect, indicating that LPS was more effectively inactivated in the oily phase of the surfactants than in water. The effect of surfactant on the hydrodynamic diameter of LPS was the same before and after steam-heat treatment for 20 minutes at 121 degrees C. Each surfactant disaggregated LPS without alteration of the activity of LPS before the heat treatment. We consider that the surfactants interact with LPS in the region of lipid A in a manner that favors loss of the activities of LPS during heating.
Chemical Phenomena↗
Prostate cancer metastasis-suppressor genes: a current perspective.
Prostate cancers account for 43% of all cancers diagnosed in American men. It is estimated that in 1996, 317,000 new cases of prostate cancer were diagnosed and 41,000 men died of the disease. The challenge of treating prostate cancer lies in accurately distinguishing those histologically-localized cancers which will complete metastatic progression from those that will remain indolent. At this time, we lack appropriate histological markers to make such distinctions, therefore, it is often difficult to accurately predict the clinical course of an individual patient's disease. There is growing evidence that a critical event in the progression of a tumor cell from a non-metastatic to metastatic phenotype is the loss of function of metastasis-suppressor genes. These genes specifically suppress the ability of a cell to metastasize. Work from several groups has demonstrated that human chromosomes 8, 10, 11 and 17 encode prostate cancer metastasis suppressor activities. As a result of these efforts the first prostate cancer metastasis-suppressor gene, KAI1, was identified and mapped to the p11-2 region of chromosome 11. In subsequent studies, an additional gene encoded by the same region, CD44 was also determined to have metastasis-suppressor activity. Recent studies have shown a correlation between decreased expression of KAI1 and CD44 and an increased malignant potential of prostate cancers. It is anticipated that the identification of other metastasis suppressor genes may allow for the development of diagnostic markers useful in the clinical substaging of individual tumors. This manuscript is intended to present our perspective on the importance of these genes in the understanding of prostate cancer progression. More importantly, we present new findings from our laboratory's effort to identify the metastasis-suppressor genes encoded by human chromosome 17. Specifically we report the strategy currently being used to evaluate a series of candidate genes and the approach being utilized to pinpoint the metastasis-suppressor region on human chromosome 17.
Animals↗