Jing Mang

Dr. Jing Mang

China-Japan Union Hospital of Jilin University

Research Focus & Metrics

Academic Career Length

22Years (2005-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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22 June 2015 in PLOS ONE
Verified
Journal Article
Open access
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YSYan-Kun Shao
Yan-Kun Shao
JMJing Mang
Jing Mang
PLPei-Lan Li
Pei-Lan Li
JWJie Wang
Jie Wang
TDTing Deng
Ting Deng
ZXZhong-Xin Xu
Zhong-Xin Xu
Several studies have assessed the effects of computer-based cognitive programs (CCP) in the management of age-related cognitive decline, but the role of CCP remains controversial. Therefore, this systematic review evaluated the evidence on the efficacy of CCP for age-related cognitive decline in healthy older adults. Six electronic databases (through October 2014) were searched. The risk of bias was assessed using the Cochrane Collaboration tool. The standardized mean difference (SMD) and 95% confidence intervals (CI) of a random-effects model were calculated. The heterogeneity was assessed using the Cochran Q statistic and quantified with the I2 index. Twelve studies were included in the current review and were considered as moderate to high methodological quality. The aggregated results indicate that CCP improves memory performance (SMD, 0.31; 95% CI 0.16 to 0.45; p < 0.0001) and processing speed (SMD, 0.50; 95% CI 0.14 to 0.87; p = 0.007) but not executive function (SMD, -0.12; 95% CI -0.33 to 0.09; p = 0.27). Furthermore, there were long-term gains in memory performance (SMD, 0.59; 95% CI 0.13 to 1.05; p = 0.01). CCP may be a valid complementary and alternative therapy for age-related cognitive decline, especially for memory performance and processing speed. However, more studies with longer follow-ups are warranted to confirm the current findings.

19 December 2021 in Bioengineered
Verified
Journal Article
Open access
RDRui Dong
Rui Dong
RHRenxuan Huang
Renxuan Huang
XSXiaohua Shi
Xiaohua Shi
ZXZhongxin Xu
Zhongxin Xu
JMJing Mang
Jing Mang
Stroke is a leading cause of morbidity and mortality worldwide. As the most common type of stroke cases, treatment effectiveness is still limited despite intensive research. Recently, traditional Chinese medicine has attracted attention because of potential benefits for stroke treatment. Among these, luteolin, a natural plant flavonoid compound, offers neuroprotection following against ischemic stroke, although the specific mechanisms are unknown. Here we used network pharmacology, molecular docking, and experimental verification to explore the mechanisms whereby luteolin can benefit stroke recovery. The pharmacological and molecular properties of luteolin were obtained from Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. The potential targets of luteolin and ischemic stroke were collected from interrogating public databases. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed by Funrich and Database for Annotation, Visualization and Integrated Discovery respectively, a luteolin-target-pathway network constructed using Cytoscape, Autodock vina was used for molecular docking simulation with Discovery Studio was used to visualize and analyze the docked conformations. Lastly, we employed an in vitro model of stroke injury to evaluate the effects of luteolin on cell survival and expression of the putative targets. From 95 candidate luteolin target genes, our analysis identified six core targets . KEGG analysis of the candidate targets identified that luteolin provides therapeutic effects on stroke through TNF signaling and other pathways. Our experimental analyses confirmed the conclusions analyzed above. In summary, the molecular and pharmacological mechanisms of luteolin against stroke are indicated in our study from a systematic perspective.

17 August 2020 in BMC Complementary Medicine and Therapies
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Journal Article
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YWYu-Kai Wang
Yu-Kai Wang
TLTie Li
Tie Li
LHLi-Juan Ha
Li-Juan Ha
ZLZhong-Wen Lv
Zhong-Wen Lv
FWFu-Chun Wang
Fu-Chun Wang
ZXZhongxin Xu
Zhongxin Xu
Background: Primary insomnia (PI) is characterized by difficulties in initiating sleep or maintaining sleep, which lead to many serious diseases. Acupuncture for PI has drawn attention with its effectiveness and safety. However, the operation of choosing acupoints lacks scientific suggestion. Our trial aims to provide reference and scientific basis for the selection of acupoints and to explore its possible mechanism. Methods: A patient-assessor-blinded, randomized and sham controlled trial was designed to compare the efficacy of 5-weeks acupuncture at a single acupoint, the combination of multi-acupoints, and a sham point. The Pittsburgh sleep quality index and Athens Insomnia Scale questionnaire were used for the primary clinical outcomes, while polysomnography was performed for the secondary clinical outcomes. The resting state functional MRI was employed to detect the cerebral responses to acupuncture. The brain activity in resting state was measured by calculating the fractional amplitude of low-frequency fluctuations (fALFF), which reflected the idiopathic activity level of neurons in the resting state. These results were analyzed by two factorial ANOVA test and post-hoc t-tests. Results: The clinical outcomes suggest that acupuncture could improve clinical symptoms, and the combination of multi-acupoints might lead to a better clinical efficacy. The rs-fMRI results suggested that the brain activity of certain regions was related to the sleep experience, and acupuncture could regulate the activity of these regions. Furthermore, the combination of multi-acupoints could impact more regions which were influenced by the sleep experience. Conclusions: Acupuncture has been proven to be beneficial for PI patients, and the combination of multi-acupoints might improve its efficacy. Trial registration: This trial has been registered on the U.S. National Library of Medicine (https://clinicaltrials.gov) ClinicalTrials.gov Identifier: NCT02448602. Registered date: 14/04/2015.

8 June 2021 in Neurology
Verified
Journal Article
Closed access
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WLWenzhao Liang
Wenzhao Liang
YWYimeng Wang
Yimeng Wang
ZDZhihua Du
Zhihua Du
JMJing Mang
Jing Mang
JWJun Wang
Jun Wang
Objective: In the real-world practice of endovascular thrombectomy (EVT) for acute ischemic stroke (AIS), the analysis of intraprocedural angiographic signs (IPASs) still challenges neurointerventionists. This review provides insights into the significance of these subtle changes for predicting underlying etiology, technical feasibility and patient prognosis, thus promoting the potential real-time application of these signs. Methods: A systematic literature search was conducted using PubMed, Ovid Medline/Embase, and Cochrane. The search focused on studies published between January 1995 and August 2020 that reported findings related to intraprocedural angiographic manifestations in endovascular recanalization therapy for AIS. Results: We identified 12 IPASs in 22 studies involving 1683 patients. The IPASs were assigned into 3 subsets according to their clinical meanings. Conclusion: The systematic analysis of IPAS in clinical trials and practice will lead to a better understanding of treatment effects, responses, and mechanisms during EVT. Studies of larger cohorts using more robust statistical methods are needed.

11 May 2021 in BMC Neurology
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Journal Article
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CWChengbing Wang
Chengbing Wang
QZQian Zhang
Qian Zhang
MJMingwei Ji
Mingwei Ji
JMJing Mang
Jing Mang
ZXZhongxin Xu
Zhongxin Xu
Background: The relationship between the neutrophil-to-lymphocyte ratio (NLR) and poor prognostics in acute ischemic stroke (AIS) patients who receive intravenous thrombolysis (IVT) remains controversial. The purpose of this systematic review and meta-analysis was to evaluate the association between the NLR and poor prognosis after IVT. Furthermore, we aimed to determine whether the NLR at admission or post-IVT plays a role in AIS patients who received IVT.Methods: The PubMed, Embase, Web of Science and China National Knowledge Infrastructure databases were searched for relevant articles until October 7, 2020. Cohort and case-control studies were included if they were related to the NLR in AIS patients treated with IVT. Odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were pooled to estimate the relationship between NLR and poor prognosis after IVT. A random effects model was used to calculate the pooled data.Results: Twelve studies, including 3641 patients, met the predefined inclusion criteria. Higher NLRs were associated with an increased risk of hemorrhagic transformation (HT) (OR = 1.33, 95 % CI = 1.14–1.56,P < 0.001) and a poor 3-month functional outcome (OR = 1.64, 95 % CI = 1.38–1.94,P < 0.001) in AIS patients who received IVT. Subgroup analysis suggested that the NLR at admission rather than post-IVT was associated with a higher risk of HT (OR = 1.33, 95 % CI = 1.01–1.75,P = 0.039). There was no statistically significant difference between higher NLRs and 3-month mortality (OR = 1.14, 95 % CI = 0.97–1.35,P = 0.120).Conclusions: A high NLR can predict HT and poor 3-month functional outcomes in AIS patients who receive IVT. The NLR at admission rather than the post-IVT NLR was an independent risk factor for an increased risk of HT after IVT.

30 December 2011 in Molecules
Verified
Journal Article
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HTHe Ting
He Ting
JMJing Mang
Jing Mang
CMChunli Mei
Chunli Mei
LYLe Yang
Le Yang
JWJiaoqi Wang
Jiaoqi Wang
ZXZhong-Xin Xu
Zhong-Xin Xu
Ischemic cerebrovascular disease is one of the most common causes of death in the World. Exogenous activin A (ActA) protects neurons against toxicity and plays a central role in regulating the brain’s response to injury. In the present study, we investigated the mechanisms involved in the neuroprotective effects of ActA in a model of hypoxic-ischemic brain disease. We found that ActA could effectively increase the survival rate of PC12 cells and relieve oxygen-glucose deprivation (OGD) damage. To clarify the neuroprotective mechanisms of ActA, the effects of ActA on the ActA/Smad pathway and on the up-regulation of inducible nitric oxide synthase (NOS) and superoxide dismutase (SOD) were investigated using OGD in PC12 cells. The results showed that ActA could increase the expression of activin receptor IIA (ActRIIA), Smad3 and Smad4 and that 50 ng/mL and 100 ng/mL of ActA could reduce NO levels and increase SOD activity by 78.9% and 79.9%, respectively. These results suggested that the neuroprotective effects of ActA in ischemia could be related to the activation of the ActA/Smad signaling pathway and to its anti-oxidant activities.