EXPERIMENTS ON ACTIVE AND PASSIVE PERMEABILITY OF BACILLUS COLI COMMUNIS*

The earlier experiments described by the writer upon the decomposition of glucose and mannitol by B. coli communis were open to the objection from the biological side that no attempt was made to distinguish those products which arose by enzyme action from those which might be more particularly associated in their formation with the growth and multiplication of the cells, and from the chemical side that certain substances of unknown composition, such as peptone, were employed, so that it was not possible to be sure that some of the products of fermentation had not been derived from this source. To overcome these objections the author has adopted a new plan of work which aims at separating the process of growth from that of fermentation.

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ORGANISMS ON THE SURFACE OF GRAIN, WITH SPECIAL REFERENCE TO BACILLUS COLI

Science ◽

10.1126/science.22.562.439 ◽

1905 ◽

Vol 22 (562) ◽

pp. 439-441 ◽

Cited By ~ 1

Author(s):

H. Metcalf

Keyword(s):

Special Reference ◽

Bacillus Coli

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SOME THEORETICAL CONSIDERATIONS UPON THE NATURE OE AGGLUTININS, TOGETHER WITH FURTHER OBSERVATIONS UPON BACILLUS TYPHI ABDOMINALIS, BACILLUS ENTERITIDIS, BACILLUS COLI COMMUNIS, BACILLUS LACTIS AEROGENES, AND SOME OTHER BACILLI OF ALLIED CHARACTER

Journal of Experimental Medicine ◽

10.1084/jem.5.4.353 ◽

1901 ◽

Vol 5 (4) ◽

pp. 353-388 ◽

Cited By ~ 15

Author(s):

Herbert E. Durham

Keyword(s):

Bacillus Coli ◽

Theoretical Considerations

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Evolution of mammalian endothermic metabolism: "leaky" membranes as a source of heat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.253.1.r1 ◽

1987 ◽

Vol 253 (1) ◽

pp. R1-R7 ◽

Cited By ~ 12

Author(s):

P. L. Else ◽

A. J. Hulbert

Keyword(s):

Cell Membrane ◽

O2 Consumption ◽

Tissue Slices ◽

Passive Permeability ◽

Mammalian Tissues ◽

Cultured Liver Cells ◽

Liver And Kidney ◽

General Difference ◽

Membrane Pumps ◽

K Transport

O2 consumption was measured at 37 degrees C in tissue slices of liver, kidney, and brain from Amphibolurus vitticeps and Rattus norvegicus (a reptile and mammal with same weight and body temperature) both in the presence and absence of ouabain. O2 consumption of the mammalian tissues was two to four times that of the reptilian tissues and the mammalian tissues used three to six times the energy for Na+-K+ transport than the reptilian tissues. Passive permeability to 42K+ was measured at 37 degrees C in liver and kidney slices, and passive permeability to 22Na+ was measured at 37 degrees C in isolated and cultured liver cells from each species. The mammalian cell membrane was severalfold "leakier" to both these ions than was the reptilian cell membrane, and thus the membrane pumps must use more energy to maintain the transmembrane ion gradients. It is postulated that this is a general difference between the cells of ectotherms and endotherms and thus partly explains the much higher levels of metabolism found in endothermic mammals.

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Lysophosphatidylcholine and sodium-calcium exchange in cardiac sarcolemma: comparison with ischemia

AJP Cell Physiology ◽

10.1152/ajpcell.1991.260.3.c433 ◽

1991 ◽

Vol 260 (3) ◽

pp. C433-C438 ◽

Cited By ~ 17

Author(s):

M. M. Bersohn ◽

K. D. Philipson ◽

R. S. Weiss

Keyword(s):

Phospholipase A2 ◽

Phospholipid Composition ◽

Maximum Velocity ◽

Passive Permeability ◽

Cardiac Sarcolemma ◽

Sodium Calcium ◽

Calcium Exchange ◽

Sarcolemmal Vesicles ◽

In Vitro Treatment

Lysophosphoglyceride accumulation in ischemic myocardium has been hypothesized to be a mechanism for altered sarcolemmal properties that underlie electrophysiological changes and Ca2+ accumulation in ischemia. We find that in vitro application of lysophosphatidylcholine to normal canine sarcolemmal vesicles at a concentration of 0.3 mumol/mg sarcolemmal protein inhibits Na(+)-Ca2+ exchange. Both maximum velocity (Vmax) for Ca2+ transport and Ca2+ affinity are reduced by lysophosphatidylcholine, whereas in ischemia only Vmax is reduced [M. M. Bersohn, K. D. Philipson, and J. Y. Fukushima. Am. J. Physiol. 242 (Cell Physiol. 11): C288-C295, 1982]. This amount of lysophosphatidylcholine does not affect sarcolemmal passive permeability to either Ca2+ or Na+. Treatment of sarcolemma with phospholipase A2 sufficient to inhibit Na(+)-Ca2+ exchange velocity by 50% causes large increases in sarcolemmal lysophosphatidylcholine and lysophosphatidylethanolamine. On the other hand, 1 h of ischemia in rabbit hearts does not affect sarcolemmal phospholipid composition. Thus, although in vitro treatment with lysophosphatidylcholine or phospholipase A2 has profound effects on sarcolemmal properties, sarcolemmal accumulation of lysophosphatidylcholine cannot account for the effects of ischemia as measured in highly purified sarcolemmal vesicles from ischemic hearts.

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