Zheng Duanmu's research while affiliated with Beijing Information Science and Technology University and other places

Ischemic vascular diseases are on the rise globally, including ischemic heart diseases, ischemic cerebrovascular diseases, and ischemic peripheral arterial diseases, posing a significant threat to life. Copper is an essential element in various biological processes, copper deficiency can reduce blood vessel elasticity and increase platelet aggregation, thereby increasing the risk of ischemic vascular disease; however, excess copper ions can lead to cytotoxicity, trigger cell death, and ultimately result in vascular injury through several signaling pathways. Herein, we review the role of cuproptosis and copper deficiency implicated in ischemic injury and repair including myocardial, cerebral, and limb ischemia. We conclude with a perspective on the therapeutic opportunities and future challenges of copper biology in understanding the pathogenesis of ischemic vascular disease states.

Flow cytometry is a versatile tool with excellent capabilities to detect and measure multiple characteristics of a population of cells or particles. Notable advancements in in vivo photoacoustic flow cytometry, coherent Raman flow cytometry, microfluidic flow cytometry, etc. have been achieved in the last two decades, which endows flow cytometry with new functions and expands its applications in basic research and clinical practice. The advanced flow cytometry broadens the tools available to researchers to conduct research involving cancer detection, microbiology (COVID-19, HIV, bacteria, etc.), and nucleic acid analysis. This review presents an overall picture of advanced flow cytometers and provides not only a clear understanding of their mechanisms but also new insights into their practical applications. We identify the latest trends in this area and aim to raise awareness of advanced techniques of flow cytometry. We hope this review expands the applications of flow cytometry and accelerates its clinical translation. This article is protected by copyright. All rights reserved.

Chemodynamic therapy (CDT) has received widespread attention due to its selectivity and oxygen independence, which is an emerging therapeutic methodology aimed at converting hydrogen peroxide (H2O2) into hydroxyl radicals (•OH)....

A novel acoustic-vibration capacitive microelectromechanical system microphone is designed, fabricated, and implemented in this paper. The new microphone consists of a rigid diaphragm and mass blocks sensitive to low-frequency vibratory and sound signals. This sensor takes advantage of the semiconductor technology to design the capacitance sensor structure by surface micromachining technology, and the inertial mass blocks are shaped using the bulk silicon micromachining technology. The structure of the anti-stiction-dimple array is designed and deployed at the bottom of the diaphragm and the backplate to avoid the risk of sensor failure by vibration stiction. The bottom and top of the backplate are designed with an anti-humidity hydrophobic insulation protective layer, which avoids adsorption of moisture and attachment of foreign particles. The thickness of the mass blocks can be controlled by the combination of the dry and the wet micromachining method, which is sensitive to different frequency responses. This study can design and produce wafer level silicon with high consistency. The inertial mass proposed in this research can be achieved through a 6 in. wafer process with >80% consistency when the thickness of the mass is around 300 μm. The sensing frequency can be reduced to below the 4 kHz frequency bandwidth with enhanced sensitivity in the ±0.5 dB range. Typical characteristic results show that the open-circuit sensitivity of the microphone is 12.63 mV/Pa (37.97 dBV/Pa) at 1 kHz (with 94 dB as the reference sound level). The total harmonic distortion and acoustic overload point are 0.21% and 121.2 dB sound pressure level, respectively. The electronic stethoscope is a typical application of this research, which can collect the characteristics and frequency spectrum of low-frequency cardiac vibration signals.

The use of traditional finite element method (FEM) in occlusal stress analysis is limited due to the complexity of musculature simulation. The present purpose was to develop a displacement boundary condition (DBC)-FEM, which evaded the muscle factor, to predict the dynamic occlusal stress. The geometry of the DBC-FEM was developed based on the scanned plastic casts obtained from a volunteer. The electrognathographic and video recorded jaw positional messages were adopted to analyze the dynamic occlusal stress. The volunteer exhibited asymmetrical lateral movements, so that the occlusal stress was further analyzed by using the parameters obtained from the right-side eccentric movement, which was 6.9 mm long, in the stress task of the left-side eccentric movement, which was 4.1 mm long. Further, virtual occlusion modification was performed by using the carving tool software aiming to improve the occlusal morphology at the loading sites. T-Scan Occlusal System was used as a control of the in vivo detection for the location and strength of the occlusal contacts. Data obtained from the calculation using the present developed DBC-FEM indicated that the stress distribution on the dental surface changed dynamically with the occlusal contacts. Consistent with the T-Scan recordings, the right-side molars always showed contacts and higher levels of stress. Replacing the left-side eccentric movement trace by the right-side one enhanced the simulated stress on the right-side molars while modification of the right-side molars reduced the simulated stress. The present DBC-FEM offers a creative approach for pragmatic occlusion stress prediction.

Background: Previous studies have indicated that the JAK/STAT signaling pathway is involved in modulating arterial adventitia inflammation response. In this study, we designed experiments to further investigate the effect of JAK2/STAT3/SOCS3 signaling in rabbit atherosclerosis process. Methods: Atherosclerosis was induced in the abdominal arteries of rabbits by balloon injury of the aorta supplemented by the atherogenic diet. Simultaneously, in the process of atherosclerosis, animals underwent either ruxolitinib treatment or not for 12 weeks. At the end of the experimental period, all rabbits were sacrificed. The plaque areas in abdominal artery, the lipid burden of plaque and the calcium burden of plaque were detected by H&E staining, Oil Red O staining and Alizarin Red staining, respectively. In addition, rabbit plasma lipids and inflammatory cytokines were measured by biochemical test kits or ELISA kits. Finally, the expression and phosphorylation levels of JAK2/STAT3/SOCS3 pathway-related proteins were detected by RT-qPCR, western blot and immunohistochemistry assays. Results: H&E staining and CT scan analysis showed that rabbit atherosclerosis model was constructed successfully. Ruxolitinib, an inhibitor of the Janus kinase 2 (JAK2), substantially reduced the area of atherosclerotic plaques in rabbits treated with high fat diet and balloon injury of the aorta. Moreover, ruxolitinib significantly decreased IL-6, IL-1β, IFN-γ and TNF-α, but increased IL-10 and IL-17 levels in plasma of atherosclerotic rabbits. Additionally, ruxolitinib reduced plasma TC, TG and LDL-C contents and AIP value, while enhanced HDL-C level in atherosclerotic rabbits. Furthermore, we found that JAK2 and STAT3 phosphorylation were up-regulated in rabbits with atherosclerosis when compared with those of the control group, followed by the expression of SOCS3 was also increased due to the activation of JAK2 and STAT3. Interestingly, ruxolitinib could inactivate JAK2 and STAT3 pathway and decrease SOCS3 expression. Conclusion: Taken together, the inhibition of JAK2/STAT3/SOCS3 signaling pathway may be a novel method for the clinical treatment of artery atherosclerosis.

Background : Previous studies have indicated that the JAK/STAT signaling pathway is involved in modulating arterial adventitia inflammation response. In this study, we designed experiment to further investigate the effect of JAK2/STAT3/SOCS3 signaling in rabbit atherosclerosis process. Methods : Atherosclerosis was induced in the abdominal arteries of rabbits by atherogenic diet and endothelial damage. At the same time, animals were received either no treatment or ruxolitinib and killed after 12 weeks. Results : H&E staining and CT scan analysis showed that rabbit atherosclerosis model was constructed successfully. Ruxolitinib, an inhibitor of the Janus kinase 2 (JAK2), substantially decreased the area of atherosclerotic plaques in rabbits treated with high fat diet and balloon injury of the aorta. Moreover, ruxolitinib substantially decreased IL-6 and TNF-α, but increased IL-10 and IL-17 levels in plasma of atherosclerotic rabbits. Additionally, ruxolitinib reduced TC and TG contents and AIP, while enhanced HDL-C level in rabbit plasma. Furthermore, we found that JAK2 and STAT3 phosphorylation were upregulated in rabbits with atherosclerosis when compared with that of the control group, and furthermore the expression of SOCS3 was also increased due to the activation of JAK2 and STAT3, while ruxolitinib inactivated JAK2 and STAT3 pathway and decreased SOCS3 expression. Conclusion : Taken together, inhibiting the JAK2/STAT3/SOCS3 signaling pathway may be a novel method for the clinical treatment of artery atherosclerosis.

Background : Previous studies have indicated that the JAK/STAT signaling pathway is involved in modulating arterial adventitia inflammation response. In this study, we designed experiment to further investigate the effect of JAK2/STAT3/SOCS3 signaling in rabbit atherosclerosis process. Methods : Atherosclerosis was induced in the abdominal arteries of rabbits by atherogenic diet and endothelial damage. At the same time, animals were received either no treatment or ruxolitinib and killed after 12 weeks. Results : H&E staining and CT scan analysis showed that rabbit atherosclerosis model was constructed successfully. Ruxolitinib, an inhibitor of the Janus kinase 2 (JAK2), substantially decreased the area of atherosclerotic plaques in rabbits treated with high fat diet and balloon injury of the aorta. Moreover, ruxolitinib substantially decreased IL-6 and TNF-α, but increased IL-10 and IL-17 levels in plasma of atherosclerotic rabbits. Additionally, ruxolitinib reduced TC and TG contents and AIP, while enhanced HDL-C level in rabbit plasma. Furthermore, we found that JAK2 and STAT3 phosphorylation were upregulated in rabbits with atherosclerosis when compared with that of the control group, and furthermore the expression of SOCS3 was also increased due to the activation of JAK2 and STAT3, while ruxolitinib inactivated JAK2 and STAT3 pathway and decreased SOCS3 expression. Conclusion : Taken together, inhibiting the JAK2/STAT3/SOCS3 signaling pathway may be a novel method for the clinical treatment of artery atherosclerosis.

Background : Previous studies have indicated that the JAK/STAT signaling pathway is involved in modulating arterial adventitia inflammation response. In this study, we designed experiment to further investigate the effect of JAK2/STAT3/SOCS3 signaling in rabbit atherosclerosis process. Methods : Atherosclerosis was induced in the abdominal arteries of rabbits by atherogenic diet and endothelial damage. At the same time, animals were received either no treatment or ruxolitinib and killed after 12 weeks. Results : H&E staining and CT scan analysis showed that rabbit atherosclerosis model was constructed successfully. Ruxolitinib, an inhibitor of the Janus kinase 2 (JAK2), substantially decreased the area of atherosclerotic plaques in rabbits treated with high fat diet and balloon injury of the aorta. Moreover, ruxolitinib substantially decreased IL-6 and TNF-α, but increased IL-10 and IL-17 levels in plasma of atherosclerotic rabbits. Additionally, ruxolitinib reduced TC and TG contents and AIP, while enhanced HDL-C level in rabbit plasma. Furthermore, we found that JAK2 and STAT3 phosphorylation were upregulated in rabbits with atherosclerosis when compared with that of the control group, and furthermore the expression of SOCS3 was also increased due to the activation of JAK2 and STAT3, while ruxolitinib inactivated JAK2 and STAT3 pathway and decreased SOCS3 expression. Conclusion : Taken together, inhibiting the JAK2/STAT3/SOCS3 signaling pathway may be a novel method for the clinical treatment of artery atherosclerosis.

One-dimensional (1D) hemodynamic models of arteries have increasingly been applied to coronary circulation. In this study, we have adopted flow and pressure profiles in Olufsen's 1D structured tree as coronary boundary conditions, with terminals coupled to the dynamic pressure feedback resulting from the intra-myocardial stress because of ventricular contraction. We model a trifurcation structure of the example coronary tree as two adjacent bifurcations. The estimated results of blood pressure and flow rate from our simulation agree well with the clinical measurements and published data. Furthermore, the 1D model enables us to use wave intensity analysis to simulate blood flow in the developed coronary model. Six characteristic waves are observed in both left and right coronary flows, though the waves' magnitudes differ from each other. We study the effects of arterial wall stiffness on coronary blood flow in the left circumflex artery (LCX). Different diseased cases indicate that distinct pathological reactions of the cardiovascular system can be better distinguished through Wave Intensity analysis, which shows agreement with clinical observations. Finally, the feedback pressure in terminal vessels and measurement deviation are also investigated by changing parameters in the LCX. We find that larger feedback pressure increases the backward wave and decreases the forward one. Although simplified, this 1D model provides new insight into coronary hemodynamics in healthy and diseased conditions. We believe that this approach offers reference resources for studies on coronary circulation disease diagnosis, treatment and simulation.