Influence of tunneling on electron screening in low energy nuclear reactions in laboratories

Using a semiclassical mean field theory, we show that the screening potential exhibits a characteristic radial variation in the tunneling region in sharp contrast to the assumption of the constant shift in all previous works. Also, we show that the explicit treatment of the tunneling region gives a larger screening energy than that in the conventional approach, which studies the time evolution only in the classical region and estimates the screening energy from the screening potential at the external classical turning point. This modification becomes important if the electronic state is not a single adiabatic state at the external turning point either by pre-tunneling transitions of the electronic state or by the symmetry of the system even if there is no essential change with the electronic state in the tunneling region.Comment: 3 figure

Structural and functional conservation of key domains in InsP3 and ryanodine receptors.

Inositol-1,4,5-trisphosphate receptors (InsP(3)Rs) and ryanodine receptors (RyRs) are tetrameric intracellular Ca(2+) channels. In each of these receptor families, the pore, which is formed by carboxy-terminal transmembrane domains, is regulated by signals that are detected by large cytosolic structures. InsP(3)R gating is initiated by InsP(3) binding to the InsP(3)-binding core (IBC, residues 224-604 of InsP(3)R1) and it requires the suppressor domain (SD, residues 1-223 of InsP(3)R1). Here we present structures of the amino-terminal region (NT, residues 1-604) of rat InsP(3)R1 with (3.6 Å) and without (3.0 Å) InsP(3) bound. The arrangement of the three NT domains, SD, IBC-β and IBC-α, identifies two discrete interfaces (α and β) between the IBC and SD. Similar interfaces occur between equivalent domains (A, B and C) in RyR1 (ref. 9). The orientations of the three domains when docked into a tetrameric structure of InsP(3)R and of the ABC domains docked into RyR are remarkably similar. The importance of the α-interface for activation of InsP(3)R and RyR is confirmed by mutagenesis and, for RyR, by disease-causing mutations. Binding of InsP(3) causes partial closure of the clam-like IBC, disrupting the β-interface and pulling the SD towards the IBC. This reorients an exposed SD loop ('hotspot' (HS) loop) that is essential for InsP(3)R activation. The loop is conserved in RyR and includes mutations that are associated with malignant hyperthermia and central core disease. The HS loop interacts with an adjacent NT, suggesting that activation re-arranges inter-subunit interactions. The A domain of RyR functionally replaced the SD in full-length InsP(3)R, and an InsP(3)R in which its C-terminal transmembrane region was replaced by that from RyR1 was gated by InsP(3) and blocked by ryanodine. Activation mechanisms are conserved between InsP(3)R and RyR. Allosteric modulation of two similar domain interfaces within an N-terminal subunit reorients the first domain (SD or A domain), allowing it, through interactions of the second domain of an adjacent subunit (IBC-β or B domain), to gate the pore

Tbx20 Is Required in Mid-Gestation Cardiomyocytes and Plays a Central Role in Atrial Development.

RationaleMutations in the transcription factor TBX20 (T-box 20) are associated with congenital heart disease. Germline ablation of Tbx20 results in abnormal heart development and embryonic lethality by embryonic day 9.5. Because Tbx20 is expressed in multiple cell lineages required for myocardial development, including pharyngeal endoderm, cardiogenic mesoderm, endocardium, and myocardium, the cell type-specific requirement for TBX20 in early myocardial development remains to be explored.ObjectiveHere, we investigated roles of TBX20 in midgestation cardiomyocytes for heart development.Methods and resultsAblation of Tbx20 from developing cardiomyocytes using a doxycycline inducible cTnTCre transgene led to embryonic lethality. The circumference of developing ventricular and atrial chambers, and in particular that of prospective left atrium, was significantly reduced in Tbx20 conditional knockout mutants. Cell cycle analysis demonstrated reduced proliferation of Tbx20 mutant cardiomyocytes and their arrest at the G1-S phase transition. Genome-wide transcriptome analysis of mutant cardiomyocytes revealed differential expression of multiple genes critical for cell cycle regulation. Moreover, atrial and ventricular gene programs seemed to be aberrantly regulated. Putative direct TBX20 targets were identified using TBX20 ChIP-Seq (chromatin immunoprecipitation with high throughput sequencing) from embryonic heart and included key cell cycle genes and atrial and ventricular specific genes. Notably, TBX20 bound a conserved enhancer for a gene key to atrial development and identity, COUP-TFII/Nr2f2 (chicken ovalbumin upstream promoter transcription factor 2/nuclear receptor subfamily 2, group F, member 2). This enhancer interacted with the NR2F2 promoter in human cardiomyocytes and conferred atrial specific gene expression in a transgenic mouse in a TBX20-dependent manner.ConclusionsMyocardial TBX20 directly regulates a subset of genes required for fetal cardiomyocyte proliferation, including those required for the G1-S transition. TBX20 also directly downregulates progenitor-specific genes and, in addition to regulating genes that specify chamber versus nonchamber myocardium, directly activates genes required for establishment or maintenance of atrial and ventricular identity. TBX20 plays a previously unappreciated key role in atrial development through direct regulation of an evolutionarily conserved COUPT-FII enhancer

Trypanosoma evansi ima gen sličan genu za oligosaharil-transferazu klona I protozoona Trypanosoma brucei rhodesiense.

Recent data has shown that there are strong indications that the putative oligosaccharyl transferase genes from Trypanosoma brucei rhodesiense were conserved within the family Trypanosomatidae. Based on these findings, the study endeavored to determine if Trypanosoma evansi also possessed putative oligosaccharyl transferase (OST) clone I previously documented in Trypanosoma brucei rhodesiense. Using the DNA hybridization method (Southern blot analyses), genomic DNAs of Trypanosoma brucei rhodesiense and Trypanosoma evansi were processed using the same set of restriction enzymes and subsequently hybridized by the same set of DNA probes designed from the reported nucleotide sequence of Trypanosoma brucei rhodesiense putative oligosaccharyl transferase clone I. The results exhibited that Trypanosoma evansi also contains a gene similar to the reported Trypanosoma brucei rhodesiense putative OST gene clone I, as shown by the successful hybridization of the DNA probes to their complementary nucleotide sequences in the genome of the Trypanosoma evansi species. In addition, the data also showed that Trypanosoma brucei rhodesiense and Trypanosoma evansi genomes shared some common restriction sites and loci within the genome of each individual parasite species.Nedavna istraživanja pokazala su da su geni za oligosaharil transferazu protozoona Trypanosoma brucei rhodesiense vrlo dobro sačuvani unutar porodice Trypanosomatidae. Cilj istraživanja bio je otkriti je li ista pojava karakteristična za gen za oligosaharil transferazu klona I protozoona Trypanosoma evansi. Genomske DNA vrste Trypanosoma brucei rhodesiense i vrste Trypanosoma evansi bile su pretražene hibridizacijom DNA (Southern Blot analizom) rabeći istu skupinu restrikcijskih enzima kao i iste probe za hibridizaciju DNA pripravljene na temelju objavljenog slijeda nukleotida za oligosaharil-transferazu klona I protozoona Trypanosoma brucei rhodesiense. Rezultati su pokazali da Trypanosoma evansi također sadrži gen koji je vrlo sličan genu za oligosaharil-transferazu protozoona Trypanosoma brucei rhodesiense, što je dokazano uspješnom hibridizacijom DNA proba s komplementarnim nukleotidnim slijedovima u genomu vrste Trypanosoma evansi. Istraživanje je pokazalo da Trypanosoma brucei rhodesiense i Trypanosoma evansi dijele i zajednička restrikcijska mjesta

Applicability of the orientation average formula in heavy-ion fusion reactions of deformed nuclei

In heavy-ion fusion reactions involving a well deformed nucleus, one often assumes that the orientation of the target nucleus does not change during the reaction. We discuss the accuracy of this procedure by analyzing the excitation function of the fusion cross section and the fusion barrier distribution in the reactions of $^{154}$Sm target with various projectiles ranging from $^{12}$C to $^{40}$Ar. It is shown that the approximation gradually looses its accuracy with increasing charge product of the projectile and target nuclei because of the effects of finite excitation energy of the target nucleus. The relevance of such inaccuracy in analyzing the experimental data is also discussed.Comment: 5 pages and 3 figure

Thermodynamic properties of ferromagnetic mixed-spin chain systems

Using a combination of high-temperature series expansion, exact diagonalization and quantum Monte Carlo, we perform a complementary analysis of the thermodynamic properties of quasi-one-dimensional mixed-spin systems with alternating magnetic moments. In addition to explicit series expansions for small spin quantum numbers, we present an expansion that allows a direct evaluation of the series coefficients as a function of spin quantum numbers. Due to the presence of excitations of both acoustic and optical nature, the specific heat of a mixed-spin chain displays a double-peak-like structure, which is more pronounced for ferromagnetic than for antiferromagnetic intra-chain exchange. We link these results to an analytically solvable half-classical limit. Finally, we extend our series expansion to incorporate the single-ion anisotropies relevant for the molecular mixed-spin ferromagnetic chain material MnNi(NO$_{2}$)$_{4}$(ethylenediamine)$_{2}$, with alternating spins of magnitude 5/2 and 1. Including a weak inter-chain coupling, we show that the observed susceptibility allows for an excellent fit, and the extraction of microscopic exchange parameters.Comment: 8 pages including 7 figures, submitted to Phys. Rev. B; series extended to 29th. QMC adde