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Increased serine phosphorylation of insulin receptor substrate-1 (IRS-1) has been proposed as a mechanism of attenuated insulin signaling in cells rendered insulin resistant by exposure to various agents such as [...]

On 13 November, 2016, an Mw7.8 earthquake occurred in Kaikoura, northern South Island, New Zealand. The Mw7.8 earthquake caused strong surface deformation, massive landslides and tsunami. Based on the fault slip model released by United States Geological Survey, the co‐seismic deformation and stress changes by Kaikoura Mw7.8 earthquake were computed with the global heterogeneous ellipsoid Earth model and high precision topography. The preliminary results show that the hanging wall of the Mw7.8 earthquake uplifted to the northeast, while the footwall subducting southwest. The co‐seismic deformation caused by this earthquake is up to several centimeters from Kaikoura to Campbell and the capital city of Wellington. The maximum co‐seismic horizontal displacement is about 1.2 m whereas the vertical is about 1.1 m. Although the accumulated strain along seismogenic faults had been released by this earthquake, the compressional force at the both ends of the seismogenic faults was increased due to co‐seismic stress changes and the maximum value of the co‐seismic stress changes reaches the order of MPa. The Coulomb failure stress changes are also up to MPa that are concentrated in the vicinity of epicenter. At the same time, the risk for NE‐SW dextral slip faults increases due to the co‐seismic shear stress. We also calculated the Coulomb Failure Stress changes in the North Island and South Island with local fault systems respectively. Our results show that Coulomb failure stress changes are positive in both regions, which means subsequent earthquakes are possible.

Chemical modification of glycerinated stalks of Vorticella with TNM is used to investigate the role of tyrosine residues in the Ca2+ -induced contraction of the spasmoneme. Tetranitromethane (TNM) is often employed as a specific reagent for the nitration of tyrosine residues in a protein at neutral and slightly alkaline pHs although TNM can also oxidize cysteine residues in the acidic and neutral pH range. Prior incubation with Ca2+ of stalks to be treated with TNM can protect the spasmoneme from irreversible denaturation. On the other hand, TNM treatment in the absence of free Ca2+ causes an irreversible denaturation of the spasmoneme. It was revealed by us that an isolated Ca2+ -binding protein called spasmin could not bind with Ca2+ after TNM treatment, even if the treatment was performed in the presence of Ca2+. In an additional experiment, we confirmed that the chemical modification of cysteine residues in the spasmoneme with N-7-dimethyl-amino-4methyl- coumarinyl- maleimide (DACM) has no effect on the contractibility. These results suggest that tyrosine residues in spasmin are essential for spasmoneme contraction and are protected from TNM in the presence of Ca2+ when spasmin binds with its receptor protein in the spasmoneme. [ABSTRACT FROM AUTHOR]

Despite great advances in lipid-lowering therapy, the gender-based disparities in lipid goal success among Chinese coronary heart disease (CHD) patients receiving lipid-lowering treatment remained uncharacterized. Furthermore, little is known about potential causes for this gender imbalance. This cross-sectional trial included 25 697 patients treated with lipid-lowering agents from 122 centres between April 2012 and October 2012; data for 9420 participants with CHD were analysed in the present study; all underwent clinical examination and had their latest fasting lipid profiles while on lipid-lowering therapy recorded. Logistic regression was used to explore possible factors associated with gender disparity in goal attainment rates, and to what extent each factor contributes. Of 9420 CHD patients (42.5% women) evaluated, women had a significantly lower overall low-density lipoprotein cholesterol (LDL-C) success rate than men (46.2 vs. 62.7%, P < 0.0001). Among CHD patients with diabetes, only 31.5% of women and 46.4% of men (P < 0.0001) attained the optional LDL-C target of <80 mg/dL. More than half (54.0%) of female patients failed to attain their non-high-density lipoprotein cholesterol (HDL-C) goal. Approximately 7.5, 8.8, 7.5, and 6.8% of gender disparity in LDL-C goal attainment rate was attributable to the gender difference in use of an anti-diabetic, anti-hypertensive, anti-platelet treatment, and the dosage of statin treatment, respectively. Although great improvements have been made over the past decade, there is still a preventive gap in high-risk and very high-risk CHD patients regarding LDL-C and non-HDL-C levels and that this gap is apparently greater in women.