排序方式: 共有5条查询结果,搜索用时 156 毫秒
1
1.
This work presents a mathematical model that establishes an interesting connection between nucleotide frequencies in human
single-stranded DNA and the famous Fibonacci’s numbers. The model relies on two assumptions. First, Chargaff’s second parity
rule should be valid, and second, the nucleotide frequencies should approach limit values when the number of bases is sufficiently
large. Under these two hypotheses, it is possible to predict the human nucleotide frequencies with accuracy. This result may
be used as evidence to the Fibonacci string model that was proposed to the sequence growth of DNA repetitive sequences. It
is noteworthy that the predicted values are solutions of an optimization problem, which is commonplace in many of nature’s
phenomena. 相似文献
2.
Kasahara DI Poynter ME Othman Z Hemenway D van der Vliet A 《Journal of immunology (Baltimore, Md. : 1950)》2008,181(1):736-745
Acrolein is a reactive unsaturated aldehyde that is produced during endogenous oxidative processes and is a major bioactive component of environmental pollutants such as cigarette smoke. Because in vitro studies demonstrate that acrolein can inhibit neutrophil apoptosis, we evaluated the effects of in vivo acrolein exposure on acute lung inflammation induced by LPS. Male C57BL/6J mice received 300 microg/kg intratracheal LPS and were exposed to acrolein (5 parts per million, 6 h/day), either before or after LPS challenge. Exposure to acrolein either before or after LPS challenge did not significantly affect the overall extent of LPS-induced lung inflammation, or the duration of the inflammatory response, as observed from recovered lung lavage leukocytes and histology. However, exposure to acrolein after LPS instillation markedly diminished the LPS-induced production of several inflammatory cytokines, specifically TNF-alpha, IL-12, and the Th1 cytokine IFN-gamma, which was associated with reduction in NF-kappaB activation. Our data demonstrate that acrolein exposure suppresses LPS-induced Th1 cytokine responses without affecting acute neutrophilia. Disruption of cytokine signaling by acrolein may represent a mechanism by which smoking contributes to chronic disease in chronic obstructive pulmonary disease and asthma. 相似文献
3.
In order to elucidate the molecular mechanism of the effect of carbon dioxide on the four-step oxygenation equilibria of hemoglobin, accurate oxygen equilibrium curves of human adult hemoglobin were determined at different concentrations of CO2 and in the presence and absence of chloride (Cl?), 2,3-diphosphoglycerate (P2G), and/or inositol hexaphosphate (IHP) and were analyzed according to Adair's stepwise oxygenation scheme to evaluate the four Adair constants, ki (i = 1 to 4). The effects of CO2 on oxygen affinity and co-operativity are influenced by H+, Cl?, P2G and IHP. The shape of the oxygen equilibrium curve varies with changes of CO2 concentration; the four Adair constants are affected by CO2 non-uniformly. Hence, the number of CO2 molecules released upon oxygenation is not the same in the individual oxygenation steps. In the absence of added Cl?, CO2 lowers the overall oxygen affinity expressed by median oxygen pressure (pm) and increases the co-operativity expressed by Hill's coefficient (nmax) by reducing k1, k2 and k3 without changing k4. significantly. The effect of CO2 on oxygen affinity becomes smaller with decrease in pH, disappearing below pH 6.5. The alkaline Bohr effect is reduced by CO2. The first oxygenation step contributes to the reduction of the Bohr effect more than the fourth step. When log pm is plotted against log [CO2] at several constant Cl? concentrations, the plots converge to a common point that is named “iso-effective point”. When log pp is plotted against log [Cl?] at several constant CO2 concentrations, the plots also converge to an iso-effective point. This phenomenon can be explained in terms of linkage relations in oxygen-linked competitive binding of CO2 and Cl?. It was found to be useful to consider in this analysis that the bicarbonate ion introduced by added CO2 exerts a heterotropic effect equivalent to that of Cl?. The combined effects of Cl?, CO2 and IHP were not explained satisfactorily by the present analysis using linkage relations. 相似文献
4.
The interaction between nitrogen oxides and hemoglobin and endothelium-derived relaxing factor 总被引:1,自引:0,他引:1
Among nitrogen oxides, NO and NO2 are free radicals and show a variety of biological effects. NO2 is a strongly oxidizing toxicant, although NO, not oxidizing as NO2, is toxic in that it interacts with hemoglobin to form nitrosyl-and methemoglobin. Nitrosylhemoglobin shows a characteristic electron spin resonance (ESR) signal due to an odd electron localized on the nitrogen atom of NO and reacts with oxygen to yield nitrate and methemoglobin, which is rapidly reduced by methemoglobin reductase in red cells. NO was found to inhibit the reductase activity. Part of NO inhaled in the body is oxidized by oxygen to NO2, which easily dissolves in water and converts to nitrite. The nitrite oxyhemoglobin autocatalytically after a lag. The mechanism of the oxidation, particularly the involvement of superoxide, was controversial. The stoichiometry of the reaction has now been established using nitrate ion electrode and a methemoglobin free radical was detected by ESR during the oxidation. Complete inhibition of the autocatalysis by aniline or aminopyrine suggests that the radical catalyzes conversion of nitrite to NO2, which oxidizes oxyhemoglobin. Recently NO was shown to be one of endothelium- derived relaxing factors and the relaxation induced by the factor was inhibited by hemoglobin and potentiated by superoxide dismutase. 相似文献
5.
1