Alteration in brain functional connectivity in patients with post-stroke cognitive impairment during memory task: A fNIRS study.

Objective: This study attempted to evaluate the functional connectivity (FC) in relevant cortex areas during three memory tasks using the functional near-infrared spectroscopy (fNIRS) method to expound the neural mechanisms in individuals with post-stroke cognitive impairment (PSCI).

Methods: Short-term memory and visuospatial abilities were assessed using the clock drawing test, digit span test, and Corsi Block-tapping tests with simultaneous fNIRS. The oxygenated hemoglobin concentration signals were recorded from the bilateral motor sense cortex (LMS/RMS) and prefrontal lobe (LPFT/PFT/RPFT) of 19 subjects with cognitive impairment (PSCI group), 27 stroke subjects (STR group) and 26 healthy subjects (HC group).

Platelet rich plasma alleviates OGD/R injury in N2a cell by enhancing autophagy through the miR‑223/PAQR3 pathway.

Our study constructed an in vitro model of cerebral ischemia/reperfusion (I/R) injury to evaluate the protective effect of platelet rich plasma (PRP) on I/R injury and uncover the mechanism behind it. Firstly, N2a cells were exposed in the condition of oxygen and glucose deprivation/reperfusion (OGD/R) to construct a model of cerebral I/R in vitro. MTT assay was employed to access the effects of PRP in N2a cell OGD/R injury.

PAQR3 protects against oxygen-glucose deprivation/reperfusion-induced injury through the ERK signaling pathway in N2A cells.

Cerebral ischemia-reperfusion injury is pivotal in the development of multiple-subcellular organelle and tissue injury after acute ischemic stroke. Recently, the Golgi apparatus (GA) has been shown to be a key subcellular organelle that plays an important role in neuroprotection against oxygen-glucose deprivation/reperfusion (OGD/R) injury. PAQR3, a scaffold protein exclusively localized in the GA, was originally discovered as a potential tumor suppressor protein.

Action of trichostatin A on Alzheimer's disease-like pathological changes in SH-SY5Y neuroblastoma cells.

The histone deacetylase inhibitor, trichostatin A, is used to treat Alzheimer's disease and can improve learning and memory but its underlying mechanism of action is unknown. To determine whether the therapeutic effect of trichostatin A on Alzheimer's disease is associated with the nuclear factor erythroid 2-related factor 2 (Nrf2) and Kelch-like epichlorohydrin-related protein-1 (Keap1) signaling pathway, amyloid β-peptide 25-35 (Aβ) was used to induce Alzheimer's disease-like pathological changes in SH-SY5Y neuroblastoma cells. Cells were then treated with trichostatin A.

Protective Effects and Mechanisms of MicroRNA-182 on Oxidative Stress in RHiN.

To explore protective effects and related mechanisms of microRNA-182 (miR-182) on oxidative stress in rat hippocampal neurons (RHiN), RHiN cells. As the results, the survival rate and superoxide dismutase levels in HO group were significantly lower than HO+miR-182 group (all P<0.05).

Genetic ablation of TAZ induces HepG2 liver cancer cell apoptosis through activating the CaMKII/MIEF1 signaling pathway.

Background And Objective: Transcriptional coactivator with PDZ-binding motif (TAZ) has been found to be associated with tumor progression. Mitochondrial homeostasis regulates cancer cell viability and metastasis. However, the roles of TAZ and mitochondrial homeostasis in liver cancer viability have not been explored.

The mechanism on phosphorylation of Hsp20Ser16 inhibit GA stress and ER stress during OGD/R.

Recent research has demonstrated that small heat shock protein (sHsp) phosphorylation plays a variety of roles in neural cells. While the phosphorylation of serine 16 (Ser16) is blocked, Hsp20 no longer has neuroprotective effects. To further investigate the mechanism underlying this process, oxygen-glucose deprivation and reperfusion (OGD/R) was used with human SH-SY5Y cells and mouse N2a neuroblastoma cells.

[Effect of high frequency electrotherapy on caspase-3 and ultra microstructure of hippocampus in rats following cerebral ischemia/reperfusion].

To investigate the effect of high frequency electrotherapy (HFE) on rat hippocampus after cerebral ischemia/reperfusion (I/R).
 Methods: A rat model of cerebral I/R injury was established. The rats were randomly divided into a sham group, an I/R group and an HFE group.

A New Approach of Short Wave Protection against Middle Cerebral Artery Occlusion/Reperfusion Injury via Attenuation of Golgi Apparatus Stress by Inhibition of Downregulation of Secretory Pathway Ca(2+)-ATPase Isoform 1 in Rats.

Background: Short wave (SW), a pattern of electromagnetic therapy, achieves an oscillating electromagnetic field. It has been reported that it may have a potential effect on cerebral injury. The present study was designed to investigate the potential role and possible mechanism of SW in focal cerebral ischemia/reperfusion (I/R) injury in rats.

Secretory pathway Ca(2+)-ATPase isoform 1 knockdown promotes Golgi apparatus stress injury in a mouse model of focal cerebral ischemia-reperfusion: In vivo and in vitro study.

The present study was designed to investigate the potential role of secretory pathway Ca(2+)-ATPase isoform 1(SPCA1) in experimental focal cerebral ischemia-reperfusion injury. Cerebral ischemia-reperfusion was induced by transient middle cerebral artery occlusion (MCAO) for 2h s in Sprague-Dawley rats, and then the expression levels of SPAC1 mRNA and protein were determined. Results showed that SPCA1 level was transiently increased 1 day after reperfusion in peri-infarction area, while markedly increased in infarction core on 3day and 7 day after reperfusion.

Characterization of Golgi scaffold proteins and their roles in compartmentalizing cell signaling.

Subcellular compartmentalization has become an important theme in cell signaling. In particular, the Golgi apparatus (GA) plays a prominent role in compartmentalizing signaling cascades that originate at the plasma membrane or other organelles. To precisely regulate this process, cells have evolved a unique class of organizer proteins, termed "scaffold proteins".