Comprehensive analysis of ceRNA network related to lincRNA in glioblastoma and prediction of clinical prognosis.

BACKGROUND: Long intergenic non-coding RNAs (lincRNAs) are capable of regulating several tumours, while competitive endogenous RNA (ceRNA) networks are of great significance in revealing the biological mechanism of tumours. Here, we aimed to study the ceRNA network of lincRNA in glioblastoma (GBM). METHODS: We obtained GBM and normal brain tissue samples from TCGA, GTEx, and GEO databases, and performed weighted gene co-expression network analysis and differential expression analysis on all lincRNA and mRNA data. Subsequently, we predicted the interaction between lincRNAs, miRNAs, and target mRNAs. Univariate and multivariate Cox regression analyses were performed on the mRNAs using CGGA data, and a Cox proportional hazards regression model was constructed. The ceRNA network was further screened by the DEmiRNA and mRNA of Cox model. RESULTS: A prognostic prediction model was constructed for patients with GBM. We assembled a ceRNA network consisting of 18 lincRNAs, 6 miRNAs, and 8 mRNAs. Gene Set Enrichment Analysis was carried out on four lincRNAs with obvious differential expressions and relatively few studies in GBM. CONCLUSION: We identified four lincRNAs that have research value for GBM and obtained the ceRNA network. Our research is expected to facilitate in-depth understanding and study of the molecular mechanism of GBM, and provide new insights into targeted therapy and prognosis of the tumour.

A physical model of a supercapacitor to reveal the mechanism of the voltage recovery phenomenon.

Quickly discharged supercapacitors are often found to show voltages that increase with time ranging from minutes to several hours. People attribute this to the special structure of the supercapacitor; however, we propose an alternative explanation. A physical model was developed to explain the phenomenon and further reveal the working mechanism of supercapacitor discharge, thus providing a guide for improving the performance of supercapacitors.

An impairment of cortical GABAergic neurons is involved in alkalosis-induced brain dysfunctions.

Acid-base imbalance leads to pathological cognition and behaviors in the clinical practices. In the comparison with acidosis, the cellular mechanisms underlying alkalosis-induced brain dysfunction remain unclear. By using electrophysiological approach, we investigated the influences of high extracellular pH environment on cortical GABAergic neurons in terms of their responsiveness to synaptic inputs and their ability to produce action potentials. Artificial cerebral spinal fluid in high pH impairs excitatory synaptic transmission and spike initiation in cortical GABAergic neurons. The alkalosis-induced dysfunction of GABAergic neurons is associated with the decrease of receptor responsiveness and the increases of spike refractory periods and threshold potentials. Our studies reveal that alkalosis impairs cortical GABAergic neurons and subsequently deteriorate brain functions. The molecular targets for alkalosis action include glutamate receptor-channels and voltage-gated sodium channels on GABAergic neurons.

Advanced glycation end products and neurodegenerative diseases: mechanisms and perspective.

The age-related neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's diseases are characterized by the abnormal accumulation or aggregation of proteins. Advanced glycation end products (AGEs) are proteins or lipids that become glycated after exposure to sugars. The formation of AGEs promotes the deposition of proteins due to the protease resistant crosslinking between the peptides and proteins. Several proteins implicated in neurodegenerative diseases such as amyloid ß, tau, α-synuclein, and prions are glycated and the extent of glycation is correlated with the pathologies of the patients. These data suggest that AGEs contribute to the development of neurodegenerative diseases. In this review we summarize recent advances on the investigation of the roles of AGEs in neurodegenerative diseases, with special focus on Alzheimer's and Parkinson's diseases. It is clear that AGEs modification triggers the abnormal deposition and accumulation of the modified proteins, which in turn sustain the local oxidative stress and inflammatory response, eventually leading to the pathological and clinical aspects of neurodegenerative diseases. Further characterization of the molecular mechanisms responsible for AGEs mediated neurotoxicity will provide important clues on the development of novel strategies for the prevention and treatment of neurodegenerative diseases.

Alkalosis leads to the over-activity of cortical principal neurons.

Alkalosis patients manifest anxiety, manic and convulsion. The elevation of mood and behavior is hypothetically a scenario that alkalosis resets the functional status of neuronal networks to overexcitation. In addition to the downregulation of inhibitory neurons, we examined whether alkalosis upregulates the functions of cortical principal neurons by electrophysiological approach. High extracellular pH condition downgrades inhibitory postsynaptic current frequency, as well as upregulates excitatory synaptic events and spike production in cortical principal neurons. Their functional upregulation is associated with the decreases of spike refractory period and threshold potential. Alkalosis downregulates GABA release from inhibitory neurons and upregulates the functions of principal neurons, which lead to imbalance between inhibitory and excitatory networks for the elevated mood and behaviors.