Publications by authors named "Dongfang Che"

Bipolar disorder (BD) is a complex psychiatric disorder characterized by dysfunctions in three domains including emotional processing, cognitive processing, and psychomotor dimensions. However, the neural underpinnings underlying these clinical profiles are not well understood. Based on the reported data, we hypothesized that (i) the core neuropathology in BD is damage in fronto-limbic network, which is associated with emotional dysfunction; (ii) changes in intrinsic brain network, such as sensorimotor network, salience network, default-mode network, central executive network are associated with impaired cognition function; and (iii) beyond the dopaminergic-driven basal ganglia-thalamo-cortical motor circuit modulated by other neurotransmitter systems, such as serotonin (subcortical-cortical modulation), the sensorimotor network and related motor function modulated by other non-motor networks such as the default-mode network are involved in psychomotor function.

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Chronic cerebral ischaemia (CCI) is a common pathological disorder, which is associated with various diseases, such as cerebral arteriosclerosis and vascular dementia, resulting in neurological dysfunction. As a type of non-coding RNA, circular RNA is involved in regulating the occurrence and development of diseases, such as ischaemic brain injury. Here, we found that HT22 cells and hippocampus treated with CCI had low expression of circ_0000296, Runx3, Sirt1, but high expression of miR-194-5p.

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Following the publication of this article, the authors realized there was an error in Figure 6H in which two versions of the figure appear.This does not impact the conclusions of the article.

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Long noncoding RNAs, a subgroup of noncoding RNAs, are implicated in ischemic brain injury. The expression levels of Snhg8, miR-384, Hoxa13, and FAM3A were measured in chronic cerebral ischemia-induced HT22 cells and hippocampal tissues. The role of the Snhg8/miR-384/Hoxa13/FAM3A axis was evaluated in chronic cerebral ischemia models in vivo and in vitro.

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Aims: The cerebellum is among the brain regions most vulnerable to damage caused by cardiac arrest, and cerebellar Purkinje cell loss may contribute to neurologic dysfunction, including post-hypoxic myoclonus. However, it remains unknown whether cerebellar Purkinje cells are protected by post-cardiac arrest therapeutic hypothermia (TH). Therefore, we examined the effect of post-cardiac arrest TH onset and duration on cerebellar Purkinje cell loss.

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Objective: Post-cardiac-arrest therapeutic hypothermia improves outcomes in comatose cardiac arrest survivors. This study tests the hypothesis that the efficacy of post-cardiac-arrest therapeutic hypothermia is dependent on the onset and duration of therapy.

Design: Prospective randomized laboratory investigation.

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Article Synopsis
  • The study investigates the specific roles of two calpain isoforms (m-calpain and micro-calpain) in neuronal damage after brain injury, focusing on their effects in live models.
  • Researchers used viral vectors to selectively reduce micro-calpain levels in adult rat hippocampal neurons, revealing that this knockdown significantly mitigated neuronal cell death and improved long-term survival after ischemic injury.
  • This is the first in vivo evidence demonstrating that targeting a specific calpain isoform can help protect brain function and reduce cell death in conditions of global brain ischemia.
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C-reactive protein (CRP) is a powerful predictor for coronary heart diseases. Recent study has revealed that adipocytes can produce CRP. Peroxisome proliferator-activated receptor (PPAR) gamma, an important nuclear transcriptional factor, can be predominately detected in adipocytes and exert several biological properties, including antiinflammatory effects.

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