The impact of cellulose nanocrystals on the aggregation and initial adhesion to a solid surface of Escherichia coli K12: Role of solution chemistry

2015 ◽  
Vol 136 ◽  
pp. 570-576 ◽  
Author(s):  
Xiaohui Sun ◽  
Yanxi Shao ◽  
Yaman Boluk ◽  
Yang Liu
Keyword(s):  
Escherichia Coli ◽  
Solid Surface ◽  
Cellulose Nanocrystals ◽  
Solution Chemistry ◽  
Escherichia Coli K12 ◽  
Initial Adhesion ◽  
The Impact

Role of Hfr Mutants in F+×F− Crosses in Escherichia coli K12

Nature ◽  
1960 ◽  
Vol 185 (4708) ◽  
pp. 265-266 ◽  
Author(s):  
P. REEVES
Keyword(s):  
Escherichia Coli ◽  
Escherichia Coli K12

High Speed Liquid Impact Onto Wetted Solid Surfaces

1994 ◽  
Vol 116 (2) ◽  
pp. 345-348 ◽  
Author(s):  
H. H. Shi ◽  
J. E. Field ◽  
C. S. J. Pickles
Keyword(s):  
Shock Wave ◽  
Liquid Layer ◽  
Solid Surface ◽  
High Speed ◽  
Shear Failure ◽  
Soda Lime ◽  
Liquid Jet ◽  
Soda Lime Glass ◽  
The Impact

The mechanics of impact by a high-speed liquid jet onto a solid surface covered by a liquid layer is described. After the liquid jet contacts the liquid layer, a shock wave is generated, which moves toward the solid surface. The shock wave is followed by the liquid jet penetrating through the layer. The influence of the liquid layer on the side jetting and stress waves is studied. Damage sites on soda-lime glass, PMMA (polymethylmethacrylate) and aluminium show the role of shear failure and cracking and provide evidence for analyzing the impact pressure on the wetted solids and the spatial pressure distribution. The liquid layer reduces the high edge impact pressures, which occur on dry targets. On wetted targets, the pressure is distributed more uniformly. Despite the cushioning effect of liquid layers, in some cases, a liquid can enhance material damage during impact due to penetration and stressing of surface cracks.

Role of the cell surface-exposed regions of outer membrane protein PhoE of Escherichia coli K12 in the biogenesis of the protein

1989 ◽  
Vol 185 (2) ◽  
pp. 365-370 ◽  
Author(s):  
Marja AGTERBERG ◽  
Henriette ADRIAANSE ◽  
Edwin TIJHAAR ◽  
Annelies RESINK ◽  
Jan TOMMASSEN
Keyword(s):  
Escherichia Coli ◽  
Membrane Protein ◽  
Cell Surface ◽  
Outer Membrane ◽  
Outer Membrane Protein ◽  
Escherichia Coli K12

Streptonigrin toxicity in Escherichia coli: oxygen dependence and the role of the intracellular oxidation–reduction state

1982 ◽  
Vol 28 (5) ◽  
pp. 545-552 ◽  
Author(s):  
John B. Harley ◽  
Caroline J. Fetterolf ◽  
Cesar A. Bello ◽  
Joel G. Flaks
Keyword(s):  
Escherichia Coli ◽  
Superoxide Dismutase ◽  
Superoxide Dismutase Activity ◽  
Lethal Concentration ◽  
Bacterial Physiology ◽  
E Coli ◽  
Escherichia Coli K12 ◽  
Oxidation Reduction

The bacterial physiology of streptonigrin toxicity was further investigated. An optimal oxygen concentration for toxicity was inferred from data showing that steptonigrin at 5 µg/mL was rapidly lethal to aerobic cultures of Escherichia coli K12 JF361, but was without effect on anaerobic cultures and was bacteriostatic to cultures incubated in 5 atm of oxygen plus 1 atm of air (5 atm O2 plus air) (1 atm = 101.325 kPa). Escherichia coli were protected from a potentially lethal concentration of streptonigrin during anaerobic incubation, whether previously grown anaerobically, aerobically, or in 5 atm O2 plus air. Superoxide dismutase activity increased with increasing oxygen tension in the medium, but was not significantly changed by a lethal concentration of streptonigrin. Although the superoxide dismutase activity was four times greater in E. coli grown in 5 atm O2 plus air than those grown in air alone, the aerobic survival in 5 µg/mL streptonigrin was identical, which suggested that superoxide dismutase was not rate limiting for toxicity. Escherichia coli K12 strains deficient in glutathione (KMBL54-129, AB1157-821, and AB1157-830) were protected from streptonigrin poisoning. Dithiothreotol (5.0 mM), diamide (1 mM), methyl viologen (1 mM), and cyanide (10 mM) protected aerobic E. coli from 5 µg/mL streptonigrin.These data are also consistent with a model of in vivo streptonigrin toxicity that requires a favorable intracellular oxidation–reduction state and an optimal concentration of molecular oxygen.

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