This mini-review is a survey of the evolution in the discovery of the primary and secondary structure of heparin. Highlights in this history include elucidation and synthesis of the specific sequence that binds to antithrombin, the development of low-molecular-weight heparins currently used as antithrombotic drugs, and the most promising start of chemo-enzymatic synthesis. Special emphasis is given to peculiar conformational properties contributing to interaction with proteins that modulate different biological properties. (C) 2014 Elsevier Ltd. All rights reserved.”
“A series of Cp*Rh-based

functional metallarectangles have been synthesized from metallaligands. Enlargement of one linker leads to the isolation of two novel Borromean link architectures. All these complexes are intact in solution, as evident from ESI-MS spectroscopic learn more analysis. Arising from the combination of open Cu centers and favorable cavity space, (Cp*Rh)(4)(bpe)(2)[Cu-(opba)center dot 2MeOH](2)4(OTf)center dot 6MeOH shows extraordinary catalytic abilities with high efficiency and wide substrate selectivity in the acyl-transfer reaction.”
“Loss of nucleoside diphosphate

kinase (Ndk) function in Escherichia coli results in an increased frequency of spontaneous mutation find more and an imbalance in dNTP pool levels. It is presumed that the imbalance in dNTP pool levels is responsible for the mutator phenotype of an E. coli ndk mutant. A human homologue of Ndk and potential suppressor of tumor metastasis, nm23-H2, can complement the mutagenic phenotype of an E: coli ndk mutant. Here, we show that the antimutagenic HIF-1 pathway property of nm23-H2 in E. coli is independent of dNTP pool levels, indicating that dNTP pool imbalance is not responsible for the mutator phenotype associated with the loss of ndk function. We have identified multiple genetic interactions between ndk and genes involved in the metabolism of dUTP, a potentially mutagenic precursor of thymidine biosynthesis. We show that loss of ndk function is synergistic with a dut-1 mutation and synthetically

lethal with the loss of thymidine kinase function. Our results suggest that Ndk prevents the accumulation of dUTP in vivo. Based on these results and biochemical studies of Ndk, we propose that the mutagenic phenotype of an ndk mutant is caused by excess misincorporation of uracil in place of thymidine combined with a defect in the uracil base excision pathway.”
“Introduction.\n\nPrevious research has suggested brain dopamine (DA) neurotransmission to be involved in the control of ejaculation. Furthermore, previous studies indicate a partly hereditary background to premature ejaculation.\n\nAim.\n\nTo investigate whether the dopamine transporter gene (DAT1) polymorphism is associated with premature ejaculation.\n\nMethods.