Long-term Blood Pressure Prediction with Deep Recurrent Neural Networks

Existing methods for arterial blood pressure (BP) estimation directly map the input physiological signals to output BP values without explicitly modeling the underlying temporal dependencies in BP dynamics. As a result, these models suffer from accuracy decay over a long time and thus require frequent calibration. In this work, we address this issue by formulating BP estimation as a sequence prediction problem in which both the input and target are temporal sequences. We propose a novel deep recurrent neural network (RNN) consisting of multilayered Long Short-Term Memory (LSTM) networks, which are incorporated with (1) a bidirectional structure to access larger-scale context information of input sequence, and (2) residual connections to allow gradients in deep RNN to propagate more effectively. The proposed deep RNN model was tested on a static BP dataset, and it achieved root mean square error (RMSE) of 3.90 and 2.66 mmHg for systolic BP (SBP) and diastolic BP (DBP) prediction respectively, surpassing the accuracy of traditional BP prediction models. On a multi-day BP dataset, the deep RNN achieved RMSE of 3.84, 5.25, 5.80 and 5.81 mmHg for the 1st day, 2nd day, 4th day and 6th month after the 1st day SBP prediction, and 1.80, 4.78, 5.0, 5.21 mmHg for corresponding DBP prediction, respectively, which outperforms all previous models with notable improvement. The experimental results suggest that modeling the temporal dependencies in BP dynamics significantly improves the long-term BP prediction accuracy.Comment: To appear in IEEE BHI 201

Phenomenological study of J/ψ→Ξ0(Λπ0)Ξˉ0(Λˉγ)J/\psi\to\Xi^0(\Lambda \pi^0) \bar{\Xi}^0(\bar{\Lambda} \gamma) decays

The measurement of decay parameters is one of the important goals of particle physics experiments, and the measurement serves as a probe to search for evidence of CP violation in baryonic decays. The experimental results will help advance existing theoretical research and establish new experimental objectives. In this paper, we formulate the asymmetric parameters that characterize parity violation, and then derive formulas for the measurement of CP violation. The formulae for the joint angular distribution of the full decay chain as well as the polarization observable of $\Xi ^ 0$, $\bar { \Xi } ^ 0$, $\Lambda$ and $\bar { \Lambda }$ are also provided for experiments. Lastly, we evaluated the sensitivity of two asymmetric parameters: $\alpha _ { \Xi ^ 0 \to \Lambda \pi ^ 0 }$ (abbreviated as $\alpha _ { \Xi ^ 0 }$) and $\alpha _ { \bar { \Xi } ^ 0 \to \bar { \Lambda } \gamma }$ (abbreviated as $\alpha_ {\bar{\Xi}^0 }$) for future experimental measurement.Comment: 8 pages, 5 figure

Dexmedetomidine post-treatment attenuates cardiac ischaemia/reperfusion injury by inhibiting apoptosis through HIF-1α signalling.

Hypoxia-inducible factor 1α (HIF-1α) plays a critical role in the apoptotic process during cardiac ischaemia/reperfusion (I/R) injury. This study aimed to investigate whether post-treatment with dexmedetomidine (DEX) could protect against I/R-induced cardiac apoptosis in vivo and in vitro via regulating HIF-1α signalling pathway. Rat myocardial I/R was induced by occluding the left anterior descending artery for 30 minutes followed by 6-hours reperfusion, and cardiomyocyte hypoxia/reoxygenation (H/R) was induced by oxygen-glucose deprivation for 6 hours followed by 3-hours reoxygenation. Dexmedetomidine administration at the beginning of reperfusion or reoxygenation attenuated I/R-induced myocardial injury or H/R-induced cell death, alleviated mitochondrial dysfunction, reduced the number of apoptotic cardiomyocytes, inhibited the activation of HIF-1α and modulated the expressions of apoptosis-related proteins including BCL-2, BAX, BNIP3, cleaved caspase-3 and cleaved PARP. Conversely, the HIF-1α prolyl hydroxylase-2 inhibitor IOX2 partly blocked DEX-mediated cardioprotection both in vivo and in vitro. Mechanistically, DEX down-regulated HIF-1α expression at the post-transcriptional level and inhibited the transcriptional activation of the target gene BNIP3. Post-treatment with DEX protects against cardiac I/R injury in vivo and H/R injury in vitro. These effects are, at least in part, mediated via the inhibition of cell apoptosis by targeting HIF-1α signalling

Ardipusilloside I induces apoptosis by regulating Bcl-2 family proteins in human mucoepidermoid carcinoma Mc3 cells

BACKGROUND: Ardisia pusilla A. DC., family Myrsinaceae, is a traditional Chinese medicine named Jiu Jie Long with a variety of pharmacological functions including anti-cancer activities. In this study, we purified a natural triterpenoid saponin, ardipusilloside I, from Ardisia pusilla, and show that it exhibits inhibitory activities in human mucoepidermoid carcinoma Mc3 cells. We also investigated the underlying mechanisms of proliferation inhibition that ardipusilloside I exerts on Mc3 cells. METHODS: MTT test was used to detect cell proliferation. Cell apoptosis was detected by transmission electron microscopy, Hoechst-33342 staining, DNA fragmentation detection, and flow cytometry. We also used western blot analysis to detect the potential mechanisms of apoptosis. RESULTS: Ardipusilloside I affected the viability of Mc3 cells in a dose- and time-dependent manner. The IC50 of ardipusilloside I was approximately 9.98 μg/ml at 48 h of treatment. Characteristic morphological changes of apoptosis, including nuclear condensation, boundary aggregation and splitting, and DNA fragmentation, were seen after treatment with 10 μg/ml ardipusilloside I for 48 h. Western blots demonstrated that ardipusilloside I caused Mc3 cell death through the induction of apoptosis by downregulation of Bcl-2 protein levels and upregulation of Bax and caspase-3 protein levels. CONCLUSIONS: Our results revealed that ardipusilloside I could be a new active substance for mucoepidermoid carcinoma treatment. We demonstrated that the potential mechanism of inhibition might be through the induction of apoptosis by regulation of Bcl-2 family protein levels. This suggests a further rationale for the development of ardipusilloside I as an anti-cancer agent

Potassium Channels in the Vascular Diseases

The vessel wall is an intricate structure composed of three layers: the intima (consisting of endothelial cells), media (consisting of smooth muscle cells and elastic fibers), and externa (consisting of the extracellular matrix scaffold). The homeostasis of the vasculature depends on the consistent function of each layer. In the vascular system, potassium channels are well known to regulate vascular function. The interactions between vascular conditions and membrane potential are complicated. In this chapter, we will focus on the functional regulation of KCa channel, KATP channel, and KV channel in the vascular system. Researchers may continuously obtain insights into the functions of these channels and identify new therapeutic targets for vascular diseases

Urinary peptidomics provides a noninvasive humanized readout of diabetic nephropathy in mice

Nephropathy is among the most frequent complications of diabetes and the leading cause of end-stage renal disease. Despite the success of novel drugs in animal models, the majority of the subsequent clinical trials employing those drugs targeting diabetic nephropathy failed. This lack of translational value may in part be due to an inadequate comparability of human disease and animal models that often capture only a few aspects of disease. Here we overcome this limitation by developing a multimolecular noninvasive humanized readout of diabetic nephropathy based on urinary peptidomics. The disease-modified urinary peptides of 2 type 2 diabetic nephropathy mouse models were identified and compared with previously validated urinary peptide markers of diabetic nephropathy in humans to generate a classifier composed of 21 ortholog peptides. This classifier predicted the response to disease and treatment with inhibitors of the renin-angiotensin system in mice. The humanized classifier was significantly correlated with glomerular lesions. Using a human type 2 diabetic validation cohort of 207 patients, the classifier also distinguished between patients with and without diabetic nephropathy, and their response to renin-angiotensin system inhibition. Thus, a combination of multiple molecular features common to both human and murine disease could provide a significant change in translational drug discovery research in type 2 diabetic nephropathy

Effects of Influent Organic Loading Rates and Electrode Locations on the Electrogenesis Capacity of Constructed Wetland-Microbial Fuel Cell Systems

Three novel constructed wetland-microbial fuel cells (CW-MFCs), based on electrode location, were developed for wastewater treatment and sustainable electricity production by embedding a MFC into a CW system. In the three CW-MFCs, electrodes were placed in different locations, including bottom anode-rhizosphere cathode CW-MFC (BA-RC-CW-MFC), rhizosphere anode-air cathode CW-MFC (RA-AC-CW-MFC), and bottom anode-air cathode CW-MFC (BA-AC-CW-MFC), to investigate the combined effects of organic loading rates (OLRs) and reactor configurations on the electrogenesis capacity of the hybrid system. All the systems operated continuously to treat five types of synthetic wastewater with increasing OLRs: 9.2, 18.4, 27.6, 55.2, and 92.0 g chemical oxygen demand (COD) m(-2) d(-1). The BA-RC-CW-MFC failed to produce electricity at any OLR, whereas the maximum power densities of 0.79 +/- 0.01 and 10.77 +/- 0.52 mW m(-2) were achieved in the RA-AC-CW-MFC with 18.4 g COD m(-2) d(-1) influent OLR and in the BA-AC-CW-MFC with 27.6 g COD m(-2) d(-1) influent OLR, respectively. The coulombic efficiencies of the RA-AC-CW-MFC and BA-AC-CW-MFC decreased gradually with the increase in influent OLRs. (C) 2016 American Institute of Chemical Engineers Environ Prog, 36: 435-441, 2017</p