P300 event-related potential component may sensitively predict mild cognitive impairment (MCI) progression. Here, pooled effect size estimates of P300 amplitude and latency were computed at midline electrodes among controls, MCI patients, and Alzheimer's disease (AD) patients. Baseline data were compared to one-year follow-up data. MCI patients showed decreased P300 amplitude and prolonged latency compared to controls. Pooled standardized mean differences (SMDs) were -0.67 (95 % CI -1.12 to -0.23, P = 0.003) and 0.90 (95 % CI 0.66-1.14, P < 0.00001), respectively. P300 latency decreased in MCI compared to AD patients where the pooled SMD was -0.52 (95 % CI -0.85 to -0.18, P = 0.003). Amplitude and latency differed between MCI baseline and follow-up. Pooled SMDs were 0.47 (95 % CI 0.29 to -0.65, P < 0.00001) and -0.52 (95 % CI -0.71 to -0.34, P < 0.00001), respectively. Group differences in MCI P300 latency existed compared to control and AD patients. P300 latency may therefore be a sensitive indicator for early cognitive decline or disease progression in MCI patients and identifying elderly patient progression to MCI and/or AD.

Glioma, like most cancers, possesses a unique bioenergetic state of aerobic glycolysis known as the Warburg effect, which is a dominant phenotype of most tumor cells. Glioma tumors exhibit high glycolytic metabolism with increased lactate production. Data derived from the gene expression profiling interactive analysis (GEPIA) database show that pyruvate dehydrogenase kinase 1 (PDK1) is significantly highly expressed in glioma tissues compared with corresponding normal tissues. PDK1 is a key enzyme in the transition of glycolysis to tricarboxylic acid cycle, via inactivating PDH and converting oxidative phosphorylation to Warburg effect, resulting in increment of lactate production. Silencing of PDK1 expression resulted in reduced lactate and ATP, accumulation of ROS, mitochondrial damage, decreased cell growth, and increased cell apoptosis. Aberrant expression of miR‐128 has been observed in many human malignancies. Mechanistically, we discover that overexpressed miR‐128‐3p disturbs the Warburg effect in glioma cells via reducing PDK1. Our experiments confirmed that the miR‐128‐3p/PDK1 axis played a pivotal role in cancer cell metabolism and growth. Collectively, these findings suggest that therapeutic strategies to modulate the Warburg effect, such as targeting of PDK1, might act as a potential therapeutic target for glioma treatment.

Background: Ischemic stroke (IS) is a common and serious neurological disease, and multiple pathways of cell apoptosis are implicated in its pathogenesis. Recently, extensive studies have indicated that pyroptosis is involved in various diseases, especially cerebrovascular diseases. However, the exact mechanism of interaction between pyroptosis and IS is scarcely understood. Thus, we aimed to investigate the impact of pyroptosis on IS-mediated systemic inflammation.Methods: First, the RNA regulation patterns mediated by 33 pyroptosis-related genes identified in 20 IS samples and 20 matched-control samples were systematically evaluated. Second, a series of bioinformatics algorithms were used to investigate the contribution of PRGs to IS pathogenesis. We determined three composition classifiers of PRGs which potentially distinguished healthy samples from IS samples according to the risk score using single-variable logistic regression, LASSO-Cox regression, and multivariable logistic regression analyses. Third, 20 IS patients were classified by unsupervised consistent cluster analysis in relation to pyroptosis. The association between pyroptosis and systemic inflammation characteristics was explored, which was inclusive of immune reaction gene sets, infiltrating immunocytes and human leukocyte antigen genes.Results: We identified that AIM2, SCAF11, and TNF can regulate immuno-inflammatory responses after strokes via the production of inflammatory factors and activation of the immune cells. Meanwhile, we identified distinct expression patterns mediated by pyroptosis and revealed their immune characteristics, differentially expressed genes, signaling pathways, and target drugs.Conclusion: Our findings lay a foundation for further research on pyroptosis and IS systemic inflammation, to improve IS prognosis and its responses to immunotherapy.

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