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Purpose Although electrocardiogram (ECG) has been proven as a biometric for human identification, applying biometric technology remains challenging with diverse heart rate circumstances in which high intensity heart rate caused waveform deformation may not be known in advance when ECG templates are registered. Methods A calibration method that calculates the ratio of the length of an unidentified electrocardiogram signal to the length of an electrocardiogram template is proposed in this paper. Next, the R peak is used as an axis anchor point of a trigonometric projection (TP) to attain the displacement value. Finally, the unidentified ECG signal is calibrated according to the generated trigonometric value, which corresponds to the trigonometric projection degree of the ratio and the attained displacement measurement. Results The results reveal that the proposed method provides superior overall performance compared with that of the conventional downsampling method, based on the percentage root mean square difference (PRD), correlation coefficients, and mean square error (MSE). Conclusion The curve fitting equation directly maps from the heart rate levels to the TP degree without prior registration information. The proposed ECG calibration method offers a more robust system against heart rate interference when conducting ECG identification.

Increasing evidence has demonstrated that excessive fructose intake induces liver fibrosis. Epithelial–mesenchymal transition (EMT) driven by transforming growth factor-β1 (TGF-β1)/mothers against decapentaplegic homolog (Smad) signaling activation promotes the occurrence and development of liver fibrosis. Magnesium isoglycyrrhizinate is clinically used as a hepatoprotective agent to treat liver fibrosis, but its underlying molecular mechanism has not been identified. Using a rat model, we found that high fructose intake reduced microRNA (miR)-375-3p expression and activated the janus-activating kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) cascade and TGF-β1/Smad signaling, which is consistent with the EMT and liver fibrosis. To further verify these observations, BRL-3A cells and/or primary rat hepatocytes were exposed to high fructose and/or transfected with a miR-375-3p mimic or inhibitor or treated with a JAK2 inhibitor, and we found that the low expression of miR-375-3p could induce the JAK2/STAT3 pathway to activate TGF-β1/Smad signaling and promote the EMT. Magnesium isoglycyrrhizinate was found to ameliorate high fructose-induced EMT and liver fibrosis in rats. More importantly, magnesium isoglycyrrhizinate increased miR-375-3p expression to suppress the JAK2/STAT3 pathway and TGF-β1/Smad signaling in these animal and cell models. This study provides evidence showing that magnesium isoglycyrrhizinate attenuates liver fibrosis associated with a high fructose diet.

Prostate cancer is a major cause of death in males. Cyproterone acetate (CPA), the steroidal anti-androgen for part of androgen deprivation therapy, may block the androgen-receptor interaction and then reduce serum testosterone through its weak anti-gonadotropic action. In addition to CPA inducing hepatitis, CPA is known to cause liver tumors in rats also. Aryl hydrocarbon receptor (AhR) is a cytoplasmic receptor and regulates multiple physiological functions. CYP1A1 is an AhR-targeted gene. We found that CPA induced CYP1A1 expression, transcriptional activity of the aryl hydrocarbon response element (AHRE), and the nuclear localization of AhR in mouse Hepa-1c1c7 cells. However, CPA suppressed CYP1A1 mRNA expression and the transcriptional activity of AHRE in human HepG2 and MCF7 cells, and also decreased AhR ligand-induced CYP1A1 protein expression and transcriptional activity of AHRE in HepG2 cells. In summary, CPA is an AhR agonist in mouse cells, but an AhR antagonist in human cells. Accordingly, CPA potentially plays a role as an endocrine disruptor of the AhR. This study helps us to understand why CPA induces acute hepatitis, gene mutation, and many other side effects. In addition, it may trigger further studies investigating the relationships between CPA, glucocorticoid receptor and castration-resistant prostate cancer in the future.

Online object tracking under complex environments is an important but challenging problem in computer vision, especially for illumination changing and occlusion conditions. With the emergence of commercial real-time depth cameras like Kinect, depth image-based object tracking, which is insensitive to illumination changing, gains more and more attentions. In this paper, we propose an online depth image-based object tracking method with sparse representation and object detection. In this framework, we combine tracking and detection to leverage precision and efficiency under heavy occlusion conditions. For tracking, objects are represented by sparse representations learned online with update. For detection, we apply two different strategies based on tracking-learning-detection and wider search window approaches. We evaluate our methods on both the subset of the public dataset Princeton Tracking Benchmark and our own driver face video in a simulated driving environment. The quantitative evaluations of precision and running time on these two datasets demonstrate the effectiveness and efficiency of our proposed object tracking algorithms.

An approach for parameter estimation of proportional-integral-derivative (PID) control system using a new nonlinear programming (NLP) algorithm was proposed. SQP/IIPM algorithm is a sequential quadratic programming (SQP) based algorithm that derives its search directions by solving quadratic programming (QP) subproblems via an infeasible interior point method (IIPM) and evaluates step length adaptively via a simple line search and/or a quadratic search algorithm depending on the termination of the IIPM solver. The task of tuning PI/PID parameters for the first- and second-order systems was modeled as constrained NLP problem. SQP/IIPM algorithm was applied to determining the optimum parameters for the PI/PID control systems. To assess the performance of the proposed method, a Matlab simulation of PID controller tuning was conducted to compare the proposed SQP/IIPM algorithm with the gain and phase margin (GPM) method and Ziegler-Nichols (ZN) method. The results reveal that, for both step and impulse response tests, the PI/PID controller using SQP/IIPM optimization algorithm consistently reduce rise time, settling-time and remarkably lower overshoot compared to GPM and ZN methods, and the proposed method improves the robustness and effectiveness of numerical optimization of PID control systems.

In this study, the variation of biomass, kinetic parameters, and stoichiometric parameters for ammonia-oxidizing bacteria (AOB) and nitrite-oxidizing bacteria (NOB) in TNCU3 process were explored at different aerobic hydraulic retention time (AHRT). The results indicated that the growth rate constants of AOB were 0.92, 0.88, and 0.95 days−1, respectively, meanwhile, those of NOB were 2.58 1.41, and 1.40 days−1, respectively, when AHRT was 5, 6, and 7 h. The lysis rate constants for AOB and NOB were 0.13 and 0.17 days−1, respectively. When AHRT was 5, 6, and 7 h, the yield coefficients of AOB were 0.20, 0.23, and 0.28 g COD g−1 N, respectively, meanwhile those of NOB were 0.23, 0.19, and 0.22 g COD g−1 N, respectively. The average percentage of AOB was 0.44, 0.61, and 0.64%, respectively, while that of NOB was 0.46, 0.61, and 0.74%, respectively. The relation between the biomass percentage of AOB and AHRT was in a good agreement with first type hyperbolic curve. The relation between the biomass percentage of NOB and AHRT was in a good agreement with seven types of curve including simple exponential curve, power exponential curve, and first type hyperbolic curve etc. When the AHRT increased from 5 to 7 h, the removal efficiency of NH4 +–N increased from 80.2 to 94.8%, or by 14.6%. Meanwhile, the removal efficiency of total nitrogen increased from 63.6 to 70.9%, or by 7.3%.

Insulin-like growth factor I (IGF-I) receptor (IGF-IR)-mediated signals are known to be involved in cell growth and transformation and prevention of apoptosis. In this study, we demonstrated the coexpression of IGF-I and IGF-IR in human esophageal carcinoma tissues. We also demonstrated the IGF-I autocrine system in esophageal carcinoma cell lines. Both the CE48T/VGH and CE81T/VGH cell lines showed proliferative responses to IGF-I stimulation. Autokinase activity of IGF-IR in these cells can be triggered by the exogenous addition of IGF-I. In addition, an IGF-I peptide antagonist, JB1, specifically inhibited ligand-induced receptor autophosphorylation in a dose-dependent manner. Under serum-free conditions, JB1 also reduced the degree of IGF-IR phosphorylation and cell numbers. Furthermore, the addition of JB1 decreased the number of CE81T/VGH colonies formed in methyl cellulose agar and the size and the incidence of tumors which grew in mice with severe combined immunodeficiency. These results imply that an IGF-I autocrine system in human esophageal carcinoma cells could stimulate tumor growth. Finally, we found that IGF-I prevented the apoptosis of CE81T/VGH cells induced by chemotherapeutic drugs, such as cisplatin, 5-fluorouracil and camptothecin. Thus, interruption of IGF-IR function may provide a way to retard tumor growth and increase the sensitivity of esophageal carcinoma to chemotherapy.