To identify patients who are likely to develop contrast-induced acute kidney injury (CI-AKI) in patients with acute myocardial infarction (AMI), a nomogram was developed in AMI patients. Totally 920 patients with AMI were enrolled in our study. The discrimination and calibration of the model were validated. External validations were also carried out in a cohort of 386 AMI patients. Our results showed in the 920 eligible AMI patients, 114 patients (21.3%) developed CI-AKI in the derivation group (n = 534), while in the validation set (n = 386), 50 patients (13%) developed CI-AKI. CI-AKI model included the following six predictors: hemoglobin, contrast volume >100 ml, hypotension before procedure, eGFR, log BNP, and age. The area under the curve (AUC) was 0.775 (95% confidence interval [CI]: 0.732–0.819) in the derivation group and 0.715 (95% CI: 0.631–0.799) in the validation group. The Hosmer-Lemeshow test has a p value of 0.557, which confirms the model’s goodness of fit. The AUC of the Mehran risk score was 0.556 (95% CI: 0.498–0.615) in the derivation group. The validated nomogram provided a useful predictive value for CI-AKI in patients with AMI.

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Objectives The objective of this study was to evaluate whether melatonin could ameliorate cognitive function in Ab 1-42 -induced mouse model and its underlying mechanisms. Methods Series behaviour tests were performed to demonstrate the amelioration of cognitive function of the Alzheimer's disease (AD) mice induced by Ab 1-42 . Additionally, enzyme-linked immunosorbent assay was applied to detect the expression of Ab 1-42 , BACE1 and p-tau protein in the brain of the AD mice. JC-1 was performed to investigate the role in alleviating mitochondrial damage by melatonin in vitro. Western blot was used to detect the expression of melatonin on apoptosis-related factors caspase-3 and Bcl-2, as well as the expressions of GSK-3b and PP2A to further determine the mechanisms of melatonin on the expression of p-tau protein.Key findings Melatonin significantly ameliorated the cognitive function and mitochondrial damage in AD mice, reduced the expression levels of GSK-3b, caspase-3, Ab 1-42 , BACE1, p-tau protein and increased the expressions of PP2A and Bcl-2. Conclusion From the overall results, we concluded that melatonin alleviated the mitochondrial damage effectively and decreased the expressions of the p-tau and some key proteins of apoptosis, leading to the improvement of cognitive function of the mice induced by Ab 1-42 .

A spintronic theory is developed to describe the effect of bias voltages on the magnetic tunnel junctions (MTJs) with a single-crystal barrier. The theory is founded on a conventional optical diffraction method and has already explained the barrier thickness effect, the temperature effect, and the half-metallic electrode effect in the MTJs with a periodic grating barrier. We find that the tunneling magnetoresistance (TMR) will oscillate with the bias voltage. This theoretical result can interpret the bias dependence observed in experiments. The range of bias voltage where the oscillations arise can be regulated by the barrier thickness and the spin polarization of the electrodes. In particular, it demonstrates that the bias voltage smaller than 100mV can hardly change the properties of TMR oscillations on the barrier thickness, which is in agreement with the experiments. Finally, a practical method is proposed to enhance and optimize the output voltage.