Barefootmacgregor5307

Using a longitudinal design, we examined whether event-related brain potentials (ERPs) correlates of successful episodic memory retrieval varied over a 4-year period according to the level of memory change. ERPs were recorded while participants performed a word-stem cued-recall task, and this procedure was repeated 4 years later. We compared the ERP old/new effect patterns of participants whose memory performance remained stable over time (stable group) with those of participants experiencing episodic memory decline (decline group). The pattern of change of the old/new effect differed between groups. At T1, the two groups exhibited the same pattern, with a positive frontal and parietal old/new effect. For the decline group, the old/new effect pattern did not change between T1 and T2. By contrast, for the stable group, the positive parietal old/new effect at T1 no longer appeared at T2, but a negative old/new effect was exhibited at frontal sites. This brain reorganization pattern could be a compensatory mechanism supporting strategic processes and allowing memory abilities to be maintained over time.

To investigate the effects of site, cerebral perfusion and degree of cerebral artery stenosis (CAS) on cognitive function.

A total of 57 patients with CAS and 53 controls from January 2019 to December 2019 were included. The former group was further divided into different subgroups according to the site, cerebral perfusion and degree of CAS. A series of neuropsychological tests were performed to evaluate the cognitive domains (such as memory, executive function, psychomotor speed, etc.). Rank sum test, t test, Chi-square test and analysis of variance were used for data analysis. Spearman correlation analysis was used to examine the relationship between the site, cerebral perfusion and degree of CAS and all tests' scores.

For patients with CAS who have decreased cerebral perfusion, their global cognitive function, memory, psychomotor speed, executive function and frontal lobe function were significantly impaired (all P < 0.05). There was a significant decrease in global cognitive function, psychomotor speed, memory, executive function and frontal lobe function in patients with anterior circulation stenosis (all P < 0.05). Moderate and severe CAS impaired subjects' global cognitive function, memory, psychomotor speed, executive function and frontal lobe function (all P < 0.05). There was a correlation between the site, cerebral perfusion, the degree of CAS and cognitive function.

Global cognitive function, memory, psychomotor speed, frontal lobe function and executive function are impaired in patients with CAS, especially in those with anterior circulatory stenosis, moderate to severe stenosis and low cerebral perfusion.See Video Abstract, http//links.lww.com/WNR/A613.

Global cognitive function, memory, psychomotor speed, frontal lobe function and executive function are impaired in patients with CAS, especially in those with anterior circulatory stenosis, moderate to severe stenosis and low cerebral perfusion.See Video Abstract, http//links.lww.com/WNR/A613.Pyroptosis has been reported to contribute to the traumatic brain injury (TBI) process. buy Telacebec Ac-FLTD-CMK is a newly synthesized pyroptosis inhibitor. However, whether Ac-FLTD-CMK inhibits pyroptosis and plays a neuroprotective role after TBI is unknown. The present study aimed to determine the effects of Ac-FLTD-CMK on TBI in a mouse model. Male C57BL/6 mice were randomly divided into sham, TBI + vehicle, and TBI + Ac-FLTD-CMK groups. TBI was induced using a weight-drop apparatus. Intraventricular injection of Ac-FLTD-CMK was performed 30 min after TBI. Caspase-1, caspase-11, gasdermin-D (GSDMD), and caspase-3 expression in the peri-contusional cortex were assessed by western blotting. Interleukin-1β (IL-1β) and interleukin-18 (IL-18) expression in the peri-contusional cortex were measured using ELISA. Behavioral experiments, brain water content, Evans blue extravasation, lactate dehydrogenase (LDH) release, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling staining were also performed. The results showed that Ac-FLTD-CMK administration significantly downregulated caspase-1 p20, caspase-11 p20, GSDMD N-terminal, IL-1β, and IL-18 expression; reduced LDH release; alleviated neuronal death; attenuated brain edema and blood-brain barrier damage; and improved neurobehavioral function. These findings indicate that Ac-FLTD-CMK treatment suppresses pyroptosis and protects mice against TBI.

This study aimed to observe the effect of glutamine (Gln) on brain damage in septic rats and explore its possible mechanism.

Ninety-three Sprague-Dawley rats were randomly divided into five groups sham operation group, sepsis group, Gln-treated group, quercetin/Gln-treated group, and alloxan/Gln-treated group. The rats in each group were continuously monitored for mean arterial pressure (MAP) and heart rate changes for 16 h. Neuroreflex scores were measured 24 h after surgery. The water content of the brain tissue was measured. Plasma neuron enolase and cysteine protease-3 were measured using the ELISA. The expression levels of heat shock protein 70 (HSP70) and oxygen-N-acetylglucosamine (O-GlcNAc) were determined by western blot analysis. Finally, the brain tissue was observed via hematoxylin and eosin staining.

The brain tissue water content, plasma neuron enolase content, brain tissue cysteine protease-3 content, and nerve reflex score were significantly lower in the Gln-treated group than in the sepsis group (P < 0.05). At the same time, the pathological brain tissue damage in the Gln-treated group was also significantly reduced. It is worth noting that the expression of HSP70 and the protein O-GlcNAc modification levels in the Gln-treated group were significantly elevated than the levels in the sepsis group (P < 0.05), and reversed by pretreatment with the HSP and O-GlcNAc inhibitors quercetion and alloxan.

Gln can attenuate brain damage in rats with sepsis, which may be associated with increased protein O-GlcNAc modification.

Gln can attenuate brain damage in rats with sepsis, which may be associated with increased protein O-GlcNAc modification.