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Zhengnian Ding

Researcher at Nanjing Medical University

Publications -  65
Citations -  1604

Zhengnian Ding is an academic researcher from Nanjing Medical University. The author has contributed to research in topics: Protein kinase B & Heat shock protein. The author has an hindex of 21, co-authored 61 publications receiving 1324 citations. Previous affiliations of Zhengnian Ding include Kanazawa University.

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Anesthesia for electroconvulsive therapy.

TL;DR: An update on the anesthetic management of patients undergoing ECT is provided to understand the physiologic responses to the electrical stimulus, the effect of anesthetic drugs on the ECT response, and the pharmacologic effects of the drugs used to attenuate the side effects related to ECT.
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Dexamethasone attenuated bupivacaine-induced neuron injury in vitro through a threonine-serine protein kinase B-dependent mechanism.

TL;DR: The data suggest that pretreatment of neuroblastoma cells with dexamethasone exerts a protective effect on bupivacaine-induced neuronal cell injury, and the mechanisms involve activating the Akt signaling pathway.
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Involvement of Reductive Stress in the Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Heat Shock Protein 27

TL;DR: The data indicate that the Hsp27-induced cardiomyopathy could be attributed to, at least in part, upregulation of glutathione peroxidase 1, and suggest that HSp27 may serve as a potential target for the treatment of patients with carduomyopathy.
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Essential role of ERK activation in neurite outgrowth induced by α-lipoic acid

TL;DR: The data suggest that LA stimulates neurite outgrowth through the activation of ERK signaling, an effect mediated through a ROS-dependent mechanism.
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Attenuation of cardiac dysfunction by HSPA12B in endotoxin-induced sepsis in mice through a PI3K-dependent mechanism.

TL;DR: It is suggested that HSPA12B plays an important role in the attenuation of endotoxin-induced cardiac dysfunction and that the mechanisms involve the preserved activation of PI3K/Akt signalling, resulting in attenuated of LPS-increased expression of VCAM-1/ICAM- 1 and leucocyte infiltration into the myocardium.