Astaxanthin in Exercise Metabolism, Performance and Recovery: A Review

During periods of heavy exercise training and competition, lipid, protein and nucleic molecules can become damaged due to an overproduction of reactive oxygen and nitrogen species within the exercising organism. As antioxidants can prevent and delay cellular oxidative damage through removing, deactivating and preventing the formation of reactive oxygen and nitrogen species, supplementation with exogenous antioxidant compounds has become a commercialised nutritional strategy commonly adopted by recreationally active individuals and athletes. The following review is written as a critical appraisal of the current literature surrounding astaxanthin and its potential application as a dietary supplement in exercising humans. Astaxanthin is a lipid-soluble antioxidant carotenoid available to supplement through the intake of Haematococcus pluvialis-derived antioxidant products. Based upon in vitro and in vivo research conducted in mice exercise models, evidence would suggest that astaxanthin supplementation could potentially improve indices of exercise metabolism, performance and recovery because of its potent antioxidant capacity. In exercising humans, however, these observations have yet to be consistently realised, with equivocal data reported. Implicated, in part, by the scarcity of well-controlled, scientifically rigorous research, future investigation is necessary to enable a more robust conclusion in regard to the efficacy of astaxanthin supplementation and its potential role in substrate utilisation, endurance performance and acute recovery in exercising humans

Context-Dependent Roles of Hes1 in the Adult Pancreas and Pancreatic Tumor Formation

[Background & Aims] The Notch signaling pathway is an important pathway in the adult pancreas and in pancreatic ductal adenocarcinoma (PDAC), with hairy and enhancer of split-1 (HES1) as the core molecule in this pathway. However, the roles of HES1 in the adult pancreas and PDAC formation remain controversial. [Methods] We used genetically engineered dual-recombinase mouse models for inducing Hes1 deletion under various conditions. [Results] The loss of Hes1 expression in the adult pancreas did not induce phenotypic alterations. However, regeneration was impaired after caerulein-induced acute pancreatitis. In a pancreatic intraepithelial neoplasia (PanIN) mouse model, PanINs rarely formed when Hes1 deletion preceded PanIN formation, whereas more PanINs were formed when Hes1 deletion succeeded PanIN formation. In a PDAC mouse model, PDAC formation was also enhanced by Hes1 deletion after PanIN/PDAC development; therefore, Hes1 promotes PanIN initiation but inhibits PanIN/PDAC progression. RNA sequencing and chromatin immunoprecipitation-quantitative polymerase chain reaction revealed that Hes1 deletion enhanced epithelial-to-mesenchymal transition via Muc5ac up-regulation in PDAC progression. The results indicated that HES1 is not required for maintaining the adult pancreas under normal conditions, but is important for regeneration during recovery from pancreatitis; moreover, Hes1 plays different roles, depending on the tumor condition. [Conclusions] Our findings highlight the context-dependent roles of HES1 in the adult pancreas and pancreatic cancer

Different mechanism of two-proton emission from proton-rich nuclei 23^{23}Al and 22^{22}Mg

Two-proton relative momentum ($q_{pp}$) and opening angle ($\theta_{pp}$) distributions from the three-body decay of two excited proton-rich nuclei, namely $^{23}$Al $\rightarrow$ p + p + $^{21}$Na and $^{22}$Mg $\rightarrow$ p + p + $^{20}$Ne, have been measured with the projectile fragment separator (RIPS) at the RIKEN RI Beam Factory. An evident peak at $q_{pp}\sim20$ MeV/c as well as a peak in $\theta_{pp}$ around 30$^\circ$ are seen in the two-proton break-up channel from a highly-excited $^{22}$Mg. In contrast, such peaks are absent for the $^{23}$Al case. It is concluded that the two-proton emission mechanism of excited $^{22}$Mg is quite different from the $^{23}$Al case, with the former having a favorable diproton emission component at a highly excited state and the latter dominated by the sequential decay process

Hindered proton collectivity in the proton-rich nucleus ^<28>S : Possible magic number Z = 16

NUCLEAR STRUCTURE AND DYNAMICS 20129–13 July 201

Hindered proton collectivity in 28S: Possible magic number at Z=16

The reduced transition probability B(E2;0 ->2+) for 28S was obtained experimentally using Coulomb excitation at 53 MeV/nucleon. The resultant B(E2) value 181(31) e2fm4 is smaller than the expectation based on empirical B(E2) systematics. The double ratio |M_n/M_p|/(N/Z) of the 0+ ->2+ transition in 28S was determined to be 1.9(2) by evaluating the M_n value from the known B(E2) value of the mirror nucleus 28Mg, showing the hindrance of proton collectivity relative to that of neutrons. These results indicate the emergence of the magic number Z=16 in the |T_z|=2 nucleus 28S.Comment: 10 pages, 3 figures. Published in Phys. Rev. Lett (http://link.aps.org/doi/10.1103/PhysRevLett.108.222501

Recent advances in glycopolypeptide synthesis

Glycosylated peptides and proteins are ubiquitous in nature and display a wide range of biological functions including mediation of recognition events, protection from proteases, and lubrication in eyes and joints. Similarly, synthetic glycopolypeptides are also expected to show great potential as biomedical materials (e.g. scaffolds for tissue repair and drug carriers), as well as serve as valuable tools for probing carbohydrate-protein interactions. Although block copolypeptides and other complex polypeptide architectures have been known for some time, the synthesis of complex and well-defined glycopolypeptide materials, until recently, has been challenging. This article reviews the many advances and accomplishments made in the past few years toward development of strategies and methods for the preparation of synthetic glycopolypeptides via ring opening polymerization. © 2014 The Royal Society of Chemistry