Shiyong Yu

Army Medical University

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Lan Huang

Sichuan University

Jianfei Chen

Chinese Academy of Agricultural Sciences

Lan Huang

Southern Medical University

Zifang Song

Huazhong University of Science and Technology

Rong Jin

Zhejiang University-University of Edinburgh Institute

Anil Nanda

Louisiana State University Health Sciences Center Shreveport

Mingbao Song

Army Medical University

D. Neil Granger

Louisiana State University Health Sciences Center Shreveport

Guohong Li

Institute of Biophysics

Xiaohui Zhao

Dairy Management

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Army Medical University

Xinqiao Hospital

Chongqing Medical University

Chinese Academy of Medical Sciences & Peking Union Medical College

Sichuan University

Shanghai Jiao Tong University

Southwest Hospital

Nanjing Medical University

Louisiana State University Health Sciences Center Shreveport

Chinese Academy of Sciences

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Abstract 200: CD40 Signaling Mediates Postischemic Inflammation, Oxidative Stress, And Tissue Injury Following Focal Cerebral Ischemia

Stroke (2012)

Rong Jin Zifang Song Shiyong Yu Daniel Daunis Brittany S Hopkins

Rationale: Although CD40/CD40 ligand (CD40L) signaling has been implicated in clinical and experimental ischemic strokes, the underlying mechanisms are largely unclear. Objective: We investigated how CD40 participates in the cellular and molecular events underlying the postischemic inflammation and oxidative stress that may contribute to the tissue damage during cerebral ischemia. Methods and Results: Wild-type (WT, n=164) and CD40 knockout mice (n=132) were subjected to middle cerebral artery occlusion (MCAO, 60 minutes) followed by reperfusion. We found that ischemia/reperfusion induced CD40 expression in the brain in a time-dependent manner, primarily localized to the microvascular endothelial cells in the early phase (6h) and then to the activated microglia in the later time (24h). The adhesion and infiltration of neutrophils as well as the activation and expansion of microglia induced by ischemia/reperfusion were inhibited in CD40-/- mice, which were time-dependently correlated with suppressing nuclear factor-kB activation and proinflammatory cytokines (IL-1β, TNFα) and adhesion molecules (E- and P-selectin, ICAM-1,MCP-1). Infarct volumes and mortality were reduced in CD40-/- mice at 72h after ischemia/reperfusion. Treatment with an inhibitor of either NADPH oxidase or COX-2, the known enzymes that contributes to the tissue damage, reduced ischemic brain injury in wild-type mice, but not in CD40-/- mice. In contrast, treatment with an inhibitor of inducible nitric oxide synthase (iNOS) further reduced tissue injury in CD40-/- mice. Consistently, ischemia/reperfusion-induced upregulation of NADPH oxidase (Nox2, and Nox4) and COX-2, but not iNOS, were attenuated in CD40-/- mice. Conclusions: The findings unveil an essential role for CD40 in the regulation of early molecular and cellular events leading to postischemic inflammation. Inhibition of CD40 signaling may be a valuable therapeutic approach to counteract the deleterious effects of postischemic inflammation.

NOX4

Proinflammatory cytokine

Brain ischemia

10.1161/str.43.suppl_1.a200

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Effect of Endurance Training on the Autonomic Nervous System Function of Young Male

International Journal of Clinical Medicine (2014)

Kaixin Tian Jun Qin Lan Huang Min Long Shiyong Yu

In this study, healthy young males were randomized into groups with moderate intensity training (n = 24), high intensity training (n = 24) and utmost intensity training (n = 24). At the end of 8-week training period, HRV measurements demonstrated a marked increase of RMSSD (P = 0.003), PNN50 (P = 0.002), HF (P = 0.002), SDNN (P = 0.002) and LF (P = 0.003) in the moderate intensity group and a decreasing tendency in LFn and LF/HF; however, in the utmost intensity group HFn (P = 0.012) decreased prominently while its LF (P = 0.032), LFn (P = 0.039) and LF/HF (P = 0.015) increased significantly. Nevertheless marked changes were not found in the above indexes of the high intensity group. While resting HR of the three groups declined significantly at the end of 8 weeks (P was 0.001, 0.0001 and 0.001 respectively); RMSSD, PNN50, HF, LF and SDNN were significantly higher in the moderate intensity group than in the other two groups (P P = 0.012) was significantly lower but its LFn and LF/HF were markedly higher (P was 0.025 and 0.015 respectively); LF/HF of both the high and utmost intensity group was significantly higher (P was 0.033 and 0.037 respectively). Despite a significant reduction of plasma NE in all the three groups at the end of 8-week training period (P was 0.016, 0, 0.031 respectively), plasma NE level of moderate and high intensity group was much lower than that of the utmost intensity group (P was 0.001, 0 respectively). Utmost and moderate endurance training results in altered sympathetic and parasympathetic balance towards sympathetic dominance and parasympathetic dominance respectively; whereas high intensity endurance training almost has no effect on ANS function. CPT and HUTT reveal the potential danger posed by utmost intensity endurance training.

Intensity

Endurance Training

10.4236/ijcm.2014.519152

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Platelet CD40 Mediates Leukocyte Recruitment and Neointima Formation after Arterial Denudation Injury in Atherosclerosis-Prone Mice

American Journal Of Pathology (2017)

Rong Jin Adam Y. Xiao Zifang Song Shiyong Yu Jarvis Li

Neointima

10.1016/j.ajpath.2017.09.007

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SDF-1α involved in mobilization and recruitment of endothelial progenitor cells after arterial injury in mice

Cardiovascular Pathology (2009)

Yangguang Yin Xiaohui Zhao Yuqiang Fang Shiyong Yu Jinghong Zhao

Homing (biology)

Neointima

Endothelial progenitor cell

10.1016/j.carpath.2009.04.002

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Lack of association of CYP11B2-344C/T polymorphism with essential hypertension: a meta-analysis.

PubMed (2015)

Jianfei Chen Jun Jing Tan H Minbao Song Shiyong Yu

A meta-analysis was carried out to evaluate the correlation between CYP11B2-344C/T polymorphism and essential hypertension susceptibility.By retrieving relevant databases and collecting domestic and international literatures about the correlation between CYP11B2-344C/T polymorphism and essential hypertension, the quality of literature were evaluated according to NEWCASTLE-OTTAWA case-control study quality rating scale (NOS). RevMan 5.0 was used to select the best genetic model, analysis the heterogeneity, calculate combined OR and the 95% CI.8532 subjects were included in this study. Compared with the control group, the OR (95% CI) values of dominant model, recessive model, and additive model were 1.01 (95% CI: 0.81~1.25), 1.03 (95% CI: 0.83~1.19) and 1.10 (95% CI: 0.93-1.29).There is no evidence to confirm that CYP11B2 (-344C/T) polymorphism is associated with susceptibility of essential hypertension.

Essential hypertension

Aldosterone synthase

genetic model

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Advanced glycation endproducts alter functions and promote apoptosis in endothelial progenitor cells through receptor for advanced glycation endproducts mediate overpression of cell oxidant stress

Molecular and Cellular Biochemistry (2009)

Jianfei Chen Minbao Song Shiyong Yu Pan Gao Yang Yu

Advanced glycation end-product

RAGE

10.1007/s11010-009-0250-y

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Citations (102)

MicroRNA Expression and Function in Cardiac Ischemic Injury

Journal of Cardiovascular Translational Research (2010)

Shiyong Yu Guohong Li

10.1007/s12265-010-9168-8

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Citations (30)

A Machine Learning Model to Predict Death Outcome in Severe COVID-19 Patients

Research Square (Research Square) (2020)

Qiao Yang Jixi Li Zhijia Zhang Xiao‐Cheng Wu Tongquan Liao

Abstract Background The novel coronavirus disease 2019 (COVID-19) spreads rapidly among people and causes a global pandemic. It is of great clinical significance to identify COVID-19 patients with high risk of death. Methods A total of 2,169 adult COVID-19 patients were enrolled from Wuhan, China between February 10th and April 15th, 2020. Difference analyses of medical records were performed between severe and non-severe groups as well as between survivors and non-survivors. In addition, we developed a decision tree classifier to identify risk factors for death outcome. Results Of the 2,169 COVID-19 patients, the median age was 61 years and male patients accounted for 48%. A total of 646 patients were diagnosed with severe illness, and 75 patients died. The most common system symptoms were respiratory, systemic and digestive symptoms. Obvious differences in demographics, clinical characteristics and laboratory examinations were found between severe and non-severe groups, as well as between survivors and non-survivors. A machine learning model was developed to predict death outcome in severe patients. The decision tree classifier included three biomarkers, neutrophil-to-lymphocyte ratio, C-reactive protein and lactic dehydrogenase. The area under the curve of the receiver operating characteristic of this model was 0.96. This model performed well both in train dataset and test dataset. The accuracy of this model was 0.98 and 0.98, respectively. Conclusion The machine learning model was robust and effective in predicting the death outcome in severe COVID-19 patients.

Demographics

10.21203/rs.3.rs-96621/v1

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Smartwatch-Based Maximum Oxygen Consumption Measurement for Predicting Acute Mountain Sickness: Diagnostic Accuracy Evaluation Study (Preprint)

Xiaowei Ye Mengjia Sun Shiyong Yu Jie Yang Zhen Liu

BACKGROUND Cardiorespiratory fitness plays an important role in coping with hypoxic stress at high altitudes. However, the association of cardiorespiratory fitness with the development of acute mountain sickness (AMS) has not yet been evaluated. Wearable technology devices provide a feasible assessment of cardiorespiratory fitness, which is quantifiable as maximum oxygen consumption (VO2max) and may contribute to AMS prediction. OBJECTIVE We aimed to determine the validity of VO2max estimated by the smartwatch test (SWT), which can be self-administered, in order to overcome the limitations of clinical VO2max measurements. We also aimed to evaluate the performance of a VO2max-SWT–based model in predicting susceptibility to AMS. METHODS Both SWT and cardiopulmonary exercise test (CPET) were performed for VO2max measurements in 46 healthy participants at low altitude (300 m) and in 41 of them at high altitude (3900 m). The characteristics of the red blood cells and hemoglobin levels in all the participants were analyzed by routine blood examination before the exercise tests. The Bland-Altman method was used for bias and precision assessment. Multivariate logistic regression was performed to analyze the correlation between AMS and the candidate variables. A receiver operating characteristic curve was used to evaluate the efficacy of VO2max in predicting AMS. RESULTS VO2max decreased after acute high altitude exposure, as measured by CPET (25.20 [SD 6.46] vs 30.17 [SD 5.01] at low altitude; P<.001) and SWT (26.17 [SD 6.71] vs 31.28 [SD 5.17] at low altitude; P<.001). Both at low and high altitudes, VO2max was slightly overestimated by SWT but had considerable accuracy as the mean absolute percentage error (<7%) and mean absolute error (<2 mL·kg–1·min–1), with a relatively small bias compared with VO2max-CPET. Twenty of the 46 participants developed AMS at 3900 m, and their VO2max was significantly lower than that of those without AMS (CPET: 27.80 [SD 4.55] vs 32.00 [SD 4.64], respectively; P=.004; SWT: 28.00 [IQR 25.25-32.00] vs 32.00 [IQR 30.00-37.00], respectively; P=.001). VO2max-CPET, VO2max-SWT, and red blood cell distribution width-coefficient of variation (RDW-CV) were found to be independent predictors of AMS. To increase the prediction accuracy, we used combination models. The combination of VO2max-SWT and RDW-CV showed the largest area under the curve for all parameters and models, which increased the area under the curve from 0.785 for VO2max-SWT alone to 0.839. CONCLUSIONS Our study demonstrates that the smartwatch device can be a feasible approach for estimating VO2max. In both low and high altitudes, VO2max-SWT showed a systematic bias toward a calibration point, slightly overestimating the proper VO2max when investigated in healthy participants. The SWT-based VO2max at low altitude is an effective indicator of AMS and helps to better identify susceptible individuals following acute high-altitude exposure, particularly by combining the RDW-CV at low altitude. CLINICALTRIAL Chinese Clinical Trial Registry ChiCTR2200059900; https://www.chictr.org.cn/showproj.html?proj=170253

Smartwatch

Ventilatory threshold

10.2196/preprints.43340

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[Effects of C-reactive protein on bone marrow-derived endothelial progenitor cell function].

Chinese journal of cardiovascular diseases (2008)

Bin Cui Lan Huang Tan H Xiaohui Zhao Mingbao Song

OBJECTIVE To observe the effects of C reactive protein (CRP) on endothelial progenitor cell (EPCs) function. METHODS Mononuclear cells (MNCs), isolated from bone marrow by density gradient centrifugation combined with adherent cell filtration, were plated on fibronectin coated culture dishes. After 7 days, adherent cells were cultured with different concentrations of CRP (0, 5, 10, 15, 20 microg/ml) for 48 hours. EPCs proliferation and migration ability were observed and adhesion assay was performed. The eNOS mRNA expression of EPCs were measured by RT-PCR. RESULTS The number of EPCs in CRP groups (10, 15, 20microg/ml) was obviously lower than that in control group (54 +/- 3, 47 +/- 3, 39 +/- 5 vs.60 +/- 3, P < 0.01). EPCs proliferation capacity was inhibited in CRP groups (10, 15, 20 microg/ml) compared with that in control group (0.297 +/- 0.036, 0.273 +/- 0.013, 0.259 +/- 0.035 vs. 0.345 +/- 0.014, P < 0.01). EPCs migration capacity was inhibited significantly in CRP groups (5, 10, 15, 20 microg/ml) than that in control group (28 +/- 2, 22 +/- 3, 19 +/- 3, 16 +/- 2 vs. 30 +/- 2, P < 0.05). EPCs adhensive number was lower in CRP groups than that in control group (11 +/- 2, 9 +/- 2, 6 +/- 2, 5 +/- 1 vs. 12 +/- 2, P < 0.05). The mRNA expressions of eNOS in CRP groups were significantly lower in control group. And compared with control group, NOS activity decreased significantly in CRP groups (10, 15, 20 microg/ml) (57.44 +/- 3.25, 48.37 +/- 3.86, 36.82 +/- 4.89 vs. 68.56 +/- 2.82, P < 0.01). CONCLUSION CRP could both reduce EPCs number and inhibit EPCs functions.

Endothelial progenitor cell

Differential centrifugation

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