No available abstract.
Leukemia, Myeloid, Acute* ; Molecular Biology* ; Translocation, Genetic*

The purpose of this study was to evaluate the changes of pre-motion time (PMT), pre-motion silent period (PMSP), and switching silent period (SSP) before and after the training using balance-mat. Twenty healthy people aged 21-36 years old (average 26.5 years old) were subjected to a series of experiment. These were randomly divided into two groups (10 subjects each), control and balance-mat group. Activities of M. Soleus and M. Tibialis anterior were recorded by electromyogram (EMG) for the duration subjects were tried to raise their both heels as quick respond to a flashing lamp. Intervention consisted of 3minutes standing on the floor in control group, and 3 minutes standing on the balance-mat in balance-mat group. Then EMG was recorded as the same manner after the intervention in each group. There was no statistical difference of duration of PMSP and SSP between the two groups before intervention. On the other hand, those in balance-mat group were significantly shorter than those in control group after intervention. In addition, in balance-mat group, duration of PMSP and SSP after intervention were significantly shorter than that before intervention. There was no statistical difference of PMT between before and after the intervention. These results suggested balance-mat training was effective for shorten the duration of SSP and PMSP, that lead to control the posture function.

The present study was designed to examine the effects of aerobic exercise on the change of alpha wave component in electroencephalogram (EEG) and plasma β-endorphin. Exercise consisted of 30-min cycling on an ergometer with the load adjusted to elicit a heart rate rise of 50% between resting and predicted maximal value. The EEG signals and blood samples were obtained before and after 30-min exercise. The EEG signal was digitized at a sampling frequency of 64 Hz and analyzed by means of computer-aided decomposition algorithm and frequency power spectral analyses, respectively. The blood samples were immediately centrifuged for 15-min for quantitative analysis of β-endorphin by means of radioimmunoassay method. Results indicated that β-endorphin was significatly (p<.05) greater after exercise as compared to that of the resting contorol. It was also found that the larger the changes in β-endorphin following exercise, the higher the appearance rate of alpha wave in EEG. There was a positive and significant correlation (r=563, p<0.05) between the increase in alpha wave component and that of the plasma β-endorphin. These results suggest that traquilizer effects of aerobic exercise could be explained, at least in part, by the increase of alpha wave component and plasma β-endorphin which in turn bring about the relaxation effects upon the central nervous system.

The present study was designed to examine the effects of aerobic exercise on the change of alpha wave component in electroencephalogram (EEG) and plasma β-endorphin. Exercise consisted of 30-min cycling on an ergometer with the load adjusted to elicit a heart rate rise of 50% between resting and predicted maximal value. The EEG signals and blood samples were obtained before and after 30-min exercise. The EEG signal was digitized at a sampling frequency of 64 Hz and analyzed by means of computer-aided decomposition algorithm and frequency power spectral analyses, respectively. The blood samples were immediately centrifuged for 15-min for quantitative analysis of β-endorphin by means of radioimmunoassay method. Results indicated that β-endorphin was significatly (p<.05) greater after exercise as compared to that of the resting contorol. It was also found that the larger the changes in β-endorphin following exercise, the higher the appearance rate of alpha wave in EEG. There was a positive and significant correlation (r=563, p<0.05) between the increase in alpha wave component and that of the plasma β-endorphin. These results suggest that traquilizer effects of aerobic exercise could be explained, at least in part, by the increase of alpha wave component and plasma β-endorphin which in turn bring about the relaxation effects upon the central nervous system.

OBJECTIVETo investigate the relationship between p73 gene and the development and progression of childhood acute lymphoblastic leukemia (ALL).

METHODSThe levels of p73 transcripts in 61 ALL cell lines and 53 childhood ALL patients were assayed using reverse transcriptase-polymerase chain reaction (RT-PCR), and their relationship with the clinicopathological characteristics was analyzed. Besides, the methylation status of p73 exon 1 was analysed by restriction-enzyme related PCR, methylation-specific PCR and bisulfite genomic sequencing in the 61 ALL cell lines.

RESULTSOf the 61 ALL cell lines, 42 showed expression of p73 mRNA, with a negative rate of 31.1%, and of the 53 primary childhood ALL samples, 39 showed expression of p73 mRNA, with a negative rate of 26.4%. Loss of p73 expression was significantly associated with the reduced disease free survival and overall survival of the patients. 39.3% (24/61) of the ALL cell lines showed hypermethylation of p73 exon 1, while normal lymphocytes and most cell lines expressed p73 mRNA were not hypermethylated.

CONCLUSIONThere was a higher negative expression rate of p73 mRNA in childhood ALL. The main mechanism of the loss expression would be the hypermethylation of p73 gene. p73 gene inactivation might play an important role in the pathogenesis of ALL. Examination of p73 mRNA might have clinical significance in predicting prognosis of childhood ALL.

Adolescent ; Cell Line ; classification ; cytology ; metabolism ; Child ; Child, Preschool ; DNA Methylation ; DNA-Binding Proteins ; genetics ; metabolism ; Disease-Free Survival ; Female ; Gene Silencing ; Genes, Tumor Suppressor ; Humans ; Infant ; Male ; Nuclear Proteins ; genetics ; metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; genetics ; metabolism ; mortality ; RNA, Messenger ; biosynthesis ; Survival Rate ; Tumor Protein p73 ; Tumor Suppressor Proteins