Exploiting barrier distributions to investigate breakup effects in the fusion of 9Be + 208Pb

Preliminary data on the fusion of 36 S + 96 Zr are reported; the excitation function near the barrier is intermediate between those of 40 Ca + 90;96 Zr. The peculiar role of the strong 3` octupole vibration of 96 Zr is pointed out, in addition to the couplings to neutron transfer channels with positive Q-values. Recent data on 40 Ca + 124 Sn are also shown; for that system the fusion barrier distribution is wide without separated peaks, similar to the case of 40 Ca + 96 Zr. Simplified coupled-channel calculations have been performed, including surface vibrations and sequential neutron pick-up channels, with form factors that fit the single- and multi-nucleon transfer data for 40 Ca + 124 Sn. A good agreement with the data is found

Origins of Incomplete Fusion Products and the Suppression of Complete Fusion in Reactions of Li 7

Above-barrier complete fusion involving nuclides with low binding energy is typically suppressed by 30%. The mechanism that causes this suppression, and produces the associated incomplete fusion products, is controversial. We have developed a new experimental approach to investigate the mechanisms that produce incomplete fusion products, combining singles and coincidence measurements of light fragments and heavy residues in 7Li + 209Bi reactions. For polonium isotopes, the dominant incomplete fusion product, only a small fraction can be explained by projectile breakup followed by capture: the dominant mechanism is triton cluster transfer. Suppression of complete fusion is therefore primarily a consequence of clustering in weakly bound nuclei rather than their breakup prior to reaching the fusion barrier. This implies that suppression of complete fusion will occur in reactions of nuclides where strong clustering is present.This work was supported by the Australian Research Council Grants No. DP170102423, No. DP160101254, and No. DP170102318

Fusion around the barrier for 7Li + 12C

Fusion cross-sections for the 7Li + 12C reaction have been measured at energies above the Coulomb barrier by the direct detection of evaporation residues. The heavy evaporation residues with energies below 3 MeV could not be separated out from the a-particles in the spectrum and hence their contribution was estimated using statistical model calculations. The present work indicates that suppression of fusion cross-sections due to the breakup of 7Li may not be significant for 7Li + 12C reaction at energies around the barrier

The genetic map and comparative analysis with the physical map of Trypanosoma brucei

Trypanosoma brucei is the causative agent of African sleeping sickness in humans and contributes to the debilitating disease ‘Nagana’ in cattle. To date we know little about the genes that determine drug resistance, host specificity, pathogenesis and virulence in these parasites. The availability of the complete genome sequence and the ability of the parasite to undergo genetic exchange have allowed genetic investigations into this parasite and here we report the first genetic map of T.brucei for the genome reference stock TREU 927, comprising of 182 markers and 11 major linkage groups, that correspond to the 11 previously identified chromosomes. The genetic map provides 90% probability of a marker being 11 cM from any given locus. Its comparison to the available physical map has revealed the average physical size of a recombination unit to be 15.6 Kb/cM. The genetic map coupled with the genome sequence and the ability to undertake crosses presents a new approach to identifying genes relevant to the disease and its prevention in this important pathogen through forward genetic analysis and positional cloning

Differences between <i>Trypanosoma brucei gambiense</i> groups 1 and 2 in their resistance to killing by Trypanolytic factor 1

&lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; The three sub-species of &lt;i&gt;Trypanosoma brucei&lt;/i&gt; are important pathogens of sub-Saharan Africa. &lt;i&gt;T. b. brucei&lt;/i&gt; is unable to infect humans due to sensitivity to trypanosome lytic factors (TLF) 1 and 2 found in human serum. &lt;i&gt;T. b. rhodesiense&lt;/i&gt; and &lt;i&gt;T. b. gambiense&lt;/i&gt; are able to resist lysis by TLF. There are two distinct sub-groups of &lt;i&gt;T. b. gambiense&lt;/i&gt; that differ genetically and by human serum resistance phenotypes. Group 1 &lt;i&gt;T. b. gambiense&lt;/i&gt; have an invariant phenotype whereas group 2 show variable resistance. Previous data indicated that group 1 &lt;i&gt;T. b. gambiense&lt;/i&gt; are resistant to TLF-1 due in-part to reduced uptake of TLF-1 mediated by reduced expression of the TLF-1 receptor (the haptoglobin-hemoglobin receptor (&lt;i&gt;HpHbR&lt;/i&gt;)) gene. Here we investigate if this is also true in group 2 parasites.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methodology:&lt;/b&gt; Isogenic resistant and sensitive group 2 &lt;i&gt;T. b. gambiense&lt;/i&gt; were derived and compared to other T. brucei parasites. Both resistant and sensitive lines express the &lt;i&gt;HpHbR&lt;/i&gt; gene at similar levels and internalized fluorescently labeled TLF-1 similar fashion to &lt;i&gt;T. b. brucei&lt;/i&gt;. Both resistant and sensitive group 2, as well as group 1 &lt;i&gt;T. b. gambiense&lt;/i&gt;, internalize recombinant APOL1, but only sensitive group 2 parasites are lysed.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusions:&lt;/b&gt; Our data indicate that, despite group 1 &lt;i&gt;T. b. gambiense&lt;/i&gt; avoiding TLF-1, it is resistant to the main lytic component, APOL1. Similarly group 2 &lt;i&gt;T. b. gambiense&lt;/i&gt; is innately resistant to APOL1, which could be based on the same mechanism. However, group 2 &lt;i&gt;T. b. gambiense&lt;/i&gt; variably displays this phenotype and expression does not appear to correlate with a change in expression site or expression of &lt;i&gt;HpHbR&lt;/i&gt;. Thus there are differences in the mechanism of human serum resistance between &lt;i&gt;T. b. gambiense&lt;/i&gt; groups 1 and 2.&lt;/p&gt

The genome sequence of <i>Trypanosoma brucei gambiense</i>, causative agent of chronic Human African Trypanosomiasis

&lt;p&gt;&lt;b&gt;Background:&lt;/b&gt; &lt;i&gt;Trypanosoma brucei gambiense&lt;/i&gt; is the causative agent of chronic Human African Trypanosomiasis or sleeping sickness, a disease endemic across often poor and rural areas of Western and Central Africa. We have previously published the genome sequence of a &lt;i&gt;T. b. brucei&lt;/i&gt; isolate, and have now employed a comparative genomics approach to understand the scale of genomic variation between &lt;i&gt;T. b. gambiense&lt;/i&gt; and the reference genome. We sought to identify features that were uniquely associated with &lt;i&gt;T. b. gambiense&lt;/i&gt; and its ability to infect humans.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods and findings:&lt;/b&gt; An improved high-quality draft genome sequence for the group 1 &lt;i&gt;T. b. gambiense&lt;/i&gt; DAL 972 isolate was produced using a whole-genome shotgun strategy. Comparison with &lt;i&gt;T. b. brucei&lt;/i&gt; showed that sequence identity averages 99.2% in coding regions, and gene order is largely collinear. However, variation associated with segmental duplications and tandem gene arrays suggests some reduction of functional repertoire in &lt;i&gt;T. b. gambiense&lt;/i&gt; DAL 972. A comparison of the variant surface glycoproteins (VSG) in &lt;i&gt;T. b. brucei&lt;/i&gt; with all &lt;i&gt;T. b. gambiense&lt;/i&gt; sequence reads showed that the essential structural repertoire of VSG domains is conserved across &lt;i&gt;T. brucei&lt;/i&gt;.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusions:&lt;/b&gt; This study provides the first estimate of intraspecific genomic variation within &lt;i&gt;T. brucei&lt;/i&gt;, and so has important consequences for future population genomics studies. We have shown that the &lt;i&gt;T. b. gambiense&lt;/i&gt; genome corresponds closely with the reference, which should therefore be an effective scaffold for any &lt;i&gt;T. brucei&lt;/i&gt; genome sequence data. As VSG repertoire is also well conserved, it may be feasible to describe the total diversity of variant antigens. While we describe several as yet uncharacterized gene families with predicted cell surface roles that were expanded in number in &lt;i&gt;T. b. brucei&lt;/i&gt;, no &lt;i&gt;T. b. gambiense&lt;/i&gt;-specific gene was identified outside of the subtelomeres that could explain the ability to infect humans.&lt;/p&gt

Systematic evidence for quasifission in 9Be-, 12C-, and 16O-induced reactions forming 258, 260No

Background: Cross sections for the formation of superheavy elements (SHE) by heavy ion fusion are suppressed by the competing quasifission process. This results in a fissionlike decay after capture but before formation of a compact compound nucleus. Fast quasifission is evident from very mass-asymmetric fission, focused in angle. In contrast, slow quasifission shows no significant mass-angle correlation, and a mass distribution peaked at symmetry. However, it shows angular distributions more anisotropic than those calculated for fission following fusion. Following fusion, low excitation energies should increase SHE survival through reduced competition from fission. However, in reactions with deformed actinide target nuclei, subbarrier fusion is highly suppressed by both fast and slow quasifission

Improved precision on the experimental E0 decay branching ratio of the Hoyle state

Background: Stellar carbon synthesis occurs exclusively via the 3α process, in which three α particles fuse to form 12C in the excited Hoyle state, followed by electromagnetic decay to the ground state. The Hoyle state is above the α threshold, and the rate of stellar carbon production depends on the radiative width of this state. The radiative width cannot be measured directly, and must instead be deduced by combining three separately measured quantities. One of these quantities is the E0 decay branching ratio of the Hoyle state, and the current 10% uncertainty on the radiative width stems mainly from the uncertainty on this ratio. The rate of the 3α process is an important input parameter in astrophysical calculations on stellar evolution, and a high precision is imperative to constrain the possible outcomes of astrophysical models.The project was supported by the Australian Research Council Discovery Grants No. DP140102986, No. DP170101673, and No. DP170102423. Operation of the ANU Heavy Ion Accelerator Facility is supported by the NCRIS HIA capability. The support from technical staff for the development of the pair spectrometer, as well as during the long experimental runs, is greatly appreciated. This work was partially supported by the International Joint Research Promotion Program of Osaka University and JSPS KAKENHI Grant No. JP 17H02893, the Natural Sciences and Engineering Research Council of Canada, the National Research Foundation (NRF), South Africa, under Grants No. 93533 and No. 118645