Cytochrome P450 monooxygenases are versatile heme-thiolate enzymes that catalyze a wide range of reactions. Self-sufficient cytochrome P450 enzymes contain the redox partners in a single polypeptide chain. Here, we present the crystal structure of full-length CYP116B46, a self-sufficient P450. The continuous polypeptide chain comprises three functional domains, which align well with the direction of electrons traveling from FMN to the heme through the [2Fe-2S] cluster. FMN and the [2Fe-2S] cluster are positioned closely, which facilitates efficient electron shuttling. The edge-to-edge straight-line distance between the [2Fe-2S] cluster and heme is approx. 25.3 Å. The role of several residues located between the [2Fe-2S] cluster and heme in the catalytic reaction is probed in mutagenesis experiments. These findings not only provide insights into the intramolecular electron transfer of self-sufficient P450s, but are also of interest for biotechnological applications of self-sufficient P450s.

Atherosclerosis is associated with multiple genetic and modifiable risk factors. There is an increasing body of evidences to indicate that epigenetic mechanisms also play an essential role in atherogenesis by influencing gene expression. Homocysteine is a sulfur-containing amino acid formed during methionine metabolism. Elevated plasma level of homocysteine is generally termed as hyperhomocysteinemia. As a potential risk factor for cardiovascular diseases, hyperhomocysteinemia may initiate or motivate atherogenesis by modification of DNA methylation. The underlying epigenetic mechanism is still unclear with controversial findings. This review focuses on epigenetic involvement and mechanisms of hyperhomocysteinemia in atherogenesis. Considering the potential beneficial effects of anti-homocysteinemia treatments in preventing atherosclerosis, further studies on the role of hyperhomocysteinemia in atherogenesis are warranted.

The thermal conductivity of the doped topological crystalline insulator, Sn0.6In0.4Te superconducting single crystal with Tc = 4.1 K, was measured down to 50 mK. It is found that the residual linear term κ0/T is negligible in zero magnetic field. The κ0/T shows a slow field dependence at low magnetic field. These results suggest that the superconducting gap is nodeless, unless there exist point nodes with directions perpendicular to the heat current. Due to its high-symmetry fcc crystal structure of Sn0.6In0.4Te, however, such point nodes can be excluded. Therefore we demonstrate that this topological superconductor candidate has a full superconducting gap in the bulk. It is likely the unconventional odd-parity A1u state which supports a surface Andreev bound state.

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A novel hybrid electrocatalyst of Co2B and Co nanoparticles immobilized on N–B-doped carbon derived from nano-B4C (Co2B/Co/N–B–C/B4C) is in situ synthesized by pyrolysis of nano-B4C supporting Co­(OH)2 nanoparticles with melamine. The Co2B and Co nanoparticles are formed and anchored on the generated N and B codoped carbon and undecomposed B4C. The hybrid exhibits remarkable catalytic performances toward the oxygen evolution reaction (OER) and oxygen reduction reaction (ORR)a very small potential of 1.53 V at 10 mA cm–2 for the OER and a high catalytic kinetics and superior durability for the ORRwhich are superior to the RuO2 and Pt/C catalyst, respectively. Most impressively, the hybrid delivers a very small potential gap of 710 mV, which is lower than those of most bifunctional electrocatalysts reported. In addition, the hybrid also shows a satisfying hydrogen evolution reaction performance offering a small overpotential of 220 mV at 10 mA cm–2 and wonderful stability. The excellent trifunctional catalytic performances issue from synergetic effects of Co2B, metal Co, Co/N-doped carbon, and B self-doped carbon coexisting in the hybrid with good interaction mutually. This work provides a new-type efficient multifunctional catalyst for regenerative fuel cell and overall water-splitting technologies.

BackgroundCyclin-dependent kinase inhibitor 2A/2B (CDKN2A/2B) near chromosome 9p21 have been associated with both atherosclerosis and artery calcification, but the underlying mechanisms remained largely unknown. Considering that CDKN2A/2B is a frequently reported site for DNA methylation, this study aimed to evaluate whether carotid artery calcification (CarAC) is related to methylation levels of CDKN2A/2B in patients with ischemic stroke.MethodsDNA methylation levels of CDKN2A/2B were measured in 322 ischemic stroke patients using peripheral blood leukocytes. Methylation levels of 36 CpG sites around promoter regions of CDKN2A/2B were examined with BiSulfite Amplicon Sequencing. CarAC was quantified with Agatston score based on results of computed tomography angiography. Generalized liner model was performed to explore the association between methylation levels and CarAC.ResultsOf the 322 analyzed patients, 187 (58.1%) were classified as with and 135 (41.9%) without evident CarAC. The average methylation levels of CDKN2B were higher in patents with CarAC than those without (5.7 vs 5.4, p = 0.001). After adjustment for potential confounders, methylation levels of CDKN2B were positively correlated with cube root transformed calcification scores (β = 0.591 ± 0.172, p = 0.001) in generalized liner model. A positive correlation was also detected between average methylation levels of CDKN2B and cube root transformed calcium volumes (β = 0.533 ± 0.160, p = 0.001).ConclusionsDNA methylation of CDKN2B may play a potential role in artery calcification.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-1093-4) contains supplementary material, which is available to authorized users.

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