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41.
Pamela M. Reilly Dr. Palmer Rogers 《Journal of industrial microbiology & biotechnology》1987,1(5):329-334
Summary Conditions that allow regeneration of cells fromClostridium acetobutylicum strain B643 protoplasts were studied. Protoplast formation and stabilization in minimal media with 50 mM CaCl2, 50 mM MgCl2 and 0.3 M sucrose were crucial to subsequent regeneration on soft yeast extract agar containing 25 mM CaCl2 and 25 mM MgCl2. A regeneration frequency of 8–25% was consistently obtained. 相似文献
42.
The acetyl-CoA pathway of autotrophic growth 总被引:3,自引:0,他引:3
Abstract The most direct conceivable route for synthesis of multicarbon compounds from CO2 is to join two molecules of CO2 together to make a 2-carbon compound and then polymerize the 2-carbon compound or add CO2 successively to the 2-carbon compound to make multicarbon compounds. Recently, it has been demonstrated that the bacterium, Clostridium thermoaceticum , grows autotrophically by such a process. The mechanism involves the reduction of one molecule of CO2 to a methyl group and then its combination with a second molecule of CO2 and CoA to form acetyl-CoA. We have designated this autotrophic pathway the acetyl-CoA pathway [1]. Evidence is accumulating that this pathway is utilized by other bacteria that grow with CO2 and H2 as the source of carbon and energy. This group includes bacteria which, like C. thermoaceticum , produce acetate as a major end product and are called acetogens or acetogenic bacteria. It also includes the methane-producing bacteria and sulfate-reducing bacteria.
The purpose of this review is to examine critically the evidence that the acetyl-CoA pathway occurs in other bacteria by a mechanism that is the same or similar to that found in C. thermoaceticum . For this purpose, the mechanism of the acetyl-CoA pathway, as found in C. thermoaceticum , is described and hypothetical mechanisms for other organisms are presented based on the acetyl-CoA pathway of C. thermoaceticum . The available data have been reviewed to determine if the hypothetical schemes are in accord with presently known facts. We conclude that the formation of acetyl-CoA by other acetogens, the methanogens and sulphate-reducing bacteria occurs by a mechanism very similar to that of C. thermoaceticum . 相似文献
The purpose of this review is to examine critically the evidence that the acetyl-CoA pathway occurs in other bacteria by a mechanism that is the same or similar to that found in C. thermoaceticum . For this purpose, the mechanism of the acetyl-CoA pathway, as found in C. thermoaceticum , is described and hypothetical mechanisms for other organisms are presented based on the acetyl-CoA pathway of C. thermoaceticum . The available data have been reviewed to determine if the hypothetical schemes are in accord with presently known facts. We conclude that the formation of acetyl-CoA by other acetogens, the methanogens and sulphate-reducing bacteria occurs by a mechanism very similar to that of C. thermoaceticum . 相似文献
43.
44.
Kevin D. Reilly 《Bulletin of mathematical biology》1968,30(4):565-579
A mathematical model for learning of a conditioned avoidance behavior is presented. An identification of the net excitation
of a neural model (Rashevsky, N., 1960.Mathematical Biophysics. Vol. II. New York: Dover Publications, Inc.) with the instantaneous probability of response is introduced and its usefulness
in discussing block-trial learning performances in the conditioned avoidance situation is outlined for normal and brain-operated
animals, using experimental data collected by the author. Later, the model is applied to consecutive trial learning and connection
is made with the approach of H. D. Landahl (1964. “An Avoidance Learning Situation. A Neural Net Model.”Bull. Math. Biophysics,26, 83–89; and 1965, “A Neural Net Model for Escape Learning.”Bull. Math. Biophysics,27, Special Edition, 317–328) wherein lie further data with which the model can be compared. 相似文献
45.
Cathepsin C: a chloride-requiring enzyme 总被引:2,自引:0,他引:2
46.
47.
48.
Linkage analysis of seven kindreds with the X-linked lymphoproliferative syndrome (XLP) confirms that the XLP locus is near DXS42 and DXS37 总被引:5,自引:0,他引:5
James C. Skare Helen L. Grierson John L. Sullivan Robert L. Nussbaum David T. Purtilo Bakary S. Sylla Gilbert M. Lenon Dorothy S. Reilly Bradley N. White Aubrey Milunsky 《Human genetics》1989,82(4):354-358
Summary Analysis of seven kindreds indicates that the XLP locus exhibits 1% recombination with DXS42 (lod = 17.5) and no recombination with DXS37 (lod = 13.3). 相似文献
49.
[3H]Glutamate uptake into astrocytes in primary culture was potently inhibited by the aspartate analoguesl- andd-aspartic acid,Dl-threo--hydroxy-aspartic acid,l-aspartic acid--hydroxymate (IC50's: 136, 259, 168, and 560 M, respectively) and by -Dl-methylene-aspartate, a suicide inhibitor of asparate aminotransferase (IC50: 524 M), and by the endogenous sulphur-containing amino acidl-cysteinesulfinic acid (IC50: 114 M). [3H]Glutamate uptake was not significantly affected by either N-methyl-d-aspartate orDl-homocysteine thiolactone. These results demonstrate that other excitatory amino acids including aspartate andl-cysteinesulfinic acid (but excludingl-homocysteic acid) interact with the glutamate transport system of astrocytes. Inhibition of glutamate uptake may significantly increase the level of neuronal excitability. 相似文献
50.
Mice bearing the H-2
bhaplotype are susceptible to the development of experimental autoimmune myasthenia gravis (EAMG), induced by acetylcholine receptor (AChR) autoimmunity. One of the genes influencing EAMG susceptibility has been mapped to the A
blocus of the major histocompatibility complex, and the A chain has been implicated in the pathogenesis. Mice of the H-2
bhaplotype, including C57BL/10 (B10), have a genomic deletion of the E
gene and therefore fail to express the E molecule on their cell surface. To test the hypothesis that failure to express the cell surface E molecule in B10 mice contributes to EAMG pathogenesis, E
inf
supk
transgenic B10 mice expressing the T molecule were examined. Expression of the E molecule in E
inf
supk
transgenic B10 mice partially prevented the development of EAMG. 相似文献