Exchange-assisted tunneling in the classical limit

The exchange interaction and correlations may produce a power-law decay instead of the usual exponential decrease of the wave function under potential barrier. The exchange-assisted tunneling vanishes in the classical limit, however, the dependence on the Planck constant h is different from that for a conventional single-particle tunneling

Effect of electron exchange on atomic ionization in a strong electric field

Hartree-Fock atom in a strong electric static field is considered. It is demonstrated that exchange between outer and inner electrons, taken into account by the so-called Fock term affects strongly the long-range behavior of the inner electron wave function. As a result, it dramatically increases its probability to be ionized. A simple model is analyzed demonstrating that the decay probability, compared to the case of a local (Hartree) atomic potential, increases by many orders of magnitude. As a result of such increase, the ratio of inner to outer electrons ionization probability became not too small. It is essential that the effect of exchange upon probability of inner electron ionization by strong electric field is proportional to the square of the number of outer electrons. It signals that in clusters the inner electron ionization by strong field, the very fact of which is manifested by e.g. high energy quanta emission, has to be essentially increased as compared to this process in gaseous atomic objects.Comment: 7 pages, 1 figur

Characterization and expression of the rat heart sarcoplasmic reticulum Ca2+-ATPase mRNA

Sarcoplasmic reticulum Ca2+-ATPase cDNA clones have been isolated from an adult rat heart cDNA library and the nucleotide sequence of the Ca2+-ATPase mRNA determined. The sequence has an open reading frame of 997 codons. It is identical to a cDNA isolated from a rat stomach cDNA library and 90% isologous to the rabbit and human slow/ cardiac cDNAs. Nuclease S1 mapping analysis indicates that this sequence corresponds to the main Ca2+-ATPase mRNA present in heart and in slow skeletal muscle and that it is expressed in various proportions in smooth and non-muscle tissues, together with another isoform which differs from the cardiac form in the sequence of its 3′-end. © 1989.link_to_subscribed_fulltex

Molecular phenotype of the hypertrophied and failing myocardium

Hemodynamic overload produces in the cardiac myocyte a complex pattern of gene reprogramming, a 'mechanogenic transduction,' characterized by qualitative and quantitative changes of gene expression. The qualitative changes involve differential expression of multigene families of contractile proteins, especially myosin heavy chain and actin, but until now, most attention has been focused on myosin heavy chain isogenes. Our recent studies were designed to characterize the pattern of expression of sarcomeric isoactins and to determine whether there is a common regulatory pathway between myosin heavy chain and actin genes. For this, we have analyzed the respective mRNA levels of α-skeletal and α-cardiac actins in human and rat ventricles during ontogeny, senescence, hypertrophy, and failure. We found that both actin isogenes are always coexpressed but that the pattern is species specific and changes depending on the situation. In man, α-skeletal actin is upregulated during development and is the predominant isoform of young and adult hearts. In rat, in contrast, α-skeletal actin is downregulated during development and after 2 months of age is expressed at a low level that does not change in aged animals. Explanted hearts from patients with end-stage heart failure exhibited the same isoactin pattern as the control ones. Comparison of all the above results with those previously reported for α- and β-myosin heavy chains indicate that myosin heavy chain and actin multigene families both are expressed in a species-specific fashion and that they are independently regulated. We have set up a run-on assay to analyze the level of regulation, transcriptional, posttranscriptional, or both, of these isogenes in 3-week-old rats and have found that their regulation is primarily transcriptional. It also appears that the transcriptional activities of the individual genes are modified during postnatal development. Quantitative changes with hemodynamic overload involve a relative decrease in the expression, without an isoform switch, of the main enzyme responsible for relaxation, the sarco(endo)plasmic reticulum ATPase, which can account, at least in part, for the alterations of calcium movements and relaxation in the hypertrophied heart. We have studied expression of this gene during the life span of rats and found that it is upregulated after birth and downregulated during aging. The overall pattern that emerges from these studies is that cardiac hypertrophy and growth, whatever the animal species, are accompanied by a very complex modulation of the genes responsible for contraction and relaxation and that it is now possible to determine the regulational level of cardiac gene expression, which should facilitate our understanding of the molecular mechanisms that result in a given phenotype and why they become ineffective during heart failure.link_to_subscribed_fulltex

Contractile proteins and sarcoplasmic reticulum calcium-ATPase gene expression in the hypertrophied and failing heart

The physiology of myocardial contractility has been studied for over a century, but only recently has molecular biology provided new insights into the mechanisms responsible for the alterations of contraction and relaxation observed during cardiac hypertrophy and heart failure. Pressure and volume overload produce in the myocyte both qualitative changes characterized by protein isoform switches and quantitative changes characterized by modulation of single genes through a mechanogenic transduction the pathways of which are largely unknown. The qualitative changes involve differential expression of multigene families of contractile proteins, especially myosin heavy chain (MHC) and actin. All situations of pressure overload, or of combined pressure and volume overload activate the β-MHC gene and deactivate the α-MHC one, which leads to a slower, more efficient contraction. In rat, pressure overload transitorily activates the α-skeletal actin gene, and both the timing and the distribution of the newly formed β-MHC and α-skeletal actin mRNAs differ. We recently found that the isoactin pattern is the same in patients with end-stage heart failure as that of control human hearts. Moreover, both in rat and human, expression of isomyosins and isoactins are not coordinated, neither during ontogeny nor senescence. All this suggests the existence of several regulatory mechanisms activated during normal cardiac growth or by a mechanical trigger, and preliminary results indicate that it is possible to perform nuclear run-on assays in order to analyze the transcriptional step of these isogenes. Relaxation of the hypertrophied heart is characterized by a relative decrease in the activity of the gene coding for the sarco(endo)plasmic reticulum ATPase (SERCA), both in rat and in man, which can explain some of the alterations of calcium handling by the hypertrophied myocyte. In conclusion, reprogramming of cardiac gene expression during ontogeny and chronic hemodynamic overloading is a complex phenomenon, and it could be hypothesized that further exploration of these genetic events may enable us to better understand how cardiac function is regulated, both in health and in disease.link_to_subscribed_fulltex