Age Differences of Quantitative Electroencephalography and Current Source Density / 신경정신의학

OBJECTIVES: Age-related differences of the brain have been obtained by various methods. This study was aimed to explore the changes of quantitative electroencephalography (qEEG) and their source localization in normal aging. METHODS: Thirty-seven healthy young adults (mean age 35.22+/-13.62 years) and thirty-nine cognitively-healthy elderly subjects (mean age 72.95+/-5.73 years) participated in the study. Resting-state EEGs were recorded while subjects were in a relaxed state. Relative qEEG powers of five frequency bands were analyzed for eye closed conditions: delta (1-3 Hz), theta (4-7 Hz), alpha (8-12 Hz), beta (13-25 Hz), and gamma (30-50 Hz). The standardized low resolution electromagnetic tomography (sLORETA) was used to identify the current source densities of each frequency band. RESULTS: The elderly group showed an increase of beta and gamma power while the reduction of delta, theta, and alpha power compared with the young group. Controlling education as a covariate, the beta power was positively correlated with age, while theta power was negatively correlated with age in all subjects. sLORETA revealed that elderly subjects had reduced current source density at the cingulate gyrus in the theta band, while increased current source densities at the frontal, parietal, insula, and limbic areas in the beta band compared with young adults. CONCLUSION: Our results suggested that qEEG could reflect normal aging. Cognitively healthy elderly subjects showed an increase of high-frequency power, while showing a reduction of low-frequency power. These functional implications were discussed.

Mechanism of Amelioration of Cisplatin Nephrotoxicity by Procaine Treatment in Mice / 대한마취과학회지

BACKGROUND: Procaine binds to DNA and reduces cisplatin nephrotoxicity, but the mechanism is poorly understood. We explored whether procaine amelioration of cisplatin nephrotoxicity was related to down-and/or up-regulation of inflammatory response gene tumor necrosis factor-alpha (TNF-alpha), oxidative stress indicator gene heme oxygenase-1 (HO-1) or cell cycle inhibitor gene p21. METHODS: Cisplatin and procaine were intraperitoneally injected to mice at a single dosage of 16 and 80 mg/kg, respectively. Renal evaluation was performed 72 hours after cisplatin administration. The expression of transcripts and proteins was analyzed using real time RT-PCR and Western blot, respectively. RESULTS: Procaine treatment moderately attenuated necrotic changes of renal proximal tubules and increases in BUN and creatinine concentration by cisplatin administration. Kidney platinum level between the cisplatin (cis) group and the cisplatin + procaine (CisPro) group was not different. Although the level of TNF-alpha mRNA increased 4-fold higher in the Cis group than in the control, this increase was not attenuated by procaine treatment. Gene expression of p21 and HO-1 was elevated 175 and 4-times higher in the Cis group than in the control, respectively. But their expression was no further elevated, rather significantly reduced in the CisPro group compared to the Cis group. Protein abundance of p21 and HO-1 was paralleled by their respective mRNA expression. CONCLUSIONS: Procaine amelioration of cisplatin nephrotoxicity is likely to be achieved through processes other than the regulation of TNF-alpha, HO-1 or p21 gene expression.