The Effects of 43 Hours of Sleep Deprivation on Executive Control Functions: Event-Related Potentials in a Visual Go/no Go Task
Qi, Jian-Lin, Shao, Yong-Cong, Miao, Danmin, Fan, Ming, Bi, Guo-Hua, Yang, Zheng, Social Behavior and Personality: an international journal
In the adult population there is a high prevalence of sleep loss which can affect physical, emotional, and cognitive functions (Falkenstein, Hoormann, & Hohnsbein, 1999; Fallgatter & Strik, 1999; Filipovic, Jahanshahi, & Rothwell, 2000). For example, workplace accidents can result from sleep loss. In order to investigate how cognitive functions are affected by sleep loss, sleep deprivation is usually used as a means to induce the state of sleep loss. Results of a number of studies on sleep have indicated that higher cognitive functions are susceptible to sleep deprivation (Diekelmann, Landolt, Lahl, Born, & Wagner, 2008; Horne, 1993; Kumar, 2008; Kuriyama, Mishima, Suzuki, Aritake, & Uchiyama, 2008; Muzur, Pace-Schott, & Hobson, 2002). It has been found that performance of tasks that rely on the prefrontal cortex are greatly affected by sleep deprivation, while performances of tasks that do not rely on frontal functions are affected less (Harrison & Horne, 2000; Horne, 1993). Such findings provide evidence for the hypothesis that the prefrontal cortex is particularly susceptible to sleep deprivation. In terms of functions rather than anatomical substrates, researchers have suggested that sleep deprivation influences frontal executive control functions in particular and the sensitivity of the prefrontal cortex to sleep has also been emphasized (Jones & Harrison, 2001; Muzur et al., 2002). In research concerning psychological cognition it has been indicated that response inhibitions, information updating, and monitoring are core aspects of executive control functions (Baddeley, 1992; Botvinick, Braver, Barch, Carter, & Cohen, 2001; D'Esposito & Grossman, 1996). Therefore, it is essential to investigate whether or not total sleep deprivation (TSD) affects executive control functions. To our knowledge, to date no event-related potentials (ERP) study has been carried out in which the aim was to assess whether or not executive control functions are impaired by 43 hours of TSD.
The Go/No-Go task (Falkenstein et al., 1999; Fallgatter & Strik, 1999; Filipovic et al., 2000) is frequently used to investigate inhibition of a response that requires activation of the executive control system. Participants are asked to produce fast responses to one kind of stimulus called Go, but to refrain from responding to another kind of stimulus called No go. In most of the Go/Nogo ERP studies it has been found that there is an N2 component for No go stimuli relative to Go stimuli, particularly at frontocentral sites (Bekker, Kenemans, & Verbaten, 2004; Fallgatter & Strik, 1999; Filipovic, Jahanshahi, & Rothwell, 1999, 2000; Nieuwenhuis, Yeung, & Cohen, 2004; Nieuwenhuis, Yeung, van den Wildenberg, & Ridderinkhof, 2004; Oddy, Barry, Johnstone, & Clarke, 2005; Scisco, Leynes, & Kang, 2008). In auditory tasks, the No go-N2 at the frontal sites close to the midline is often found to be smaller compared with the No go-N2 that is elicited by visual stimulation (Falkenstein et al., 1999; Falkenstein et al., 2002; Tekok-Kilic, Shucard, & Shucard, 2001). A P300 was also found at frontal and central sites which was larger for No go than that for Go (Falkenstein et al., 1999; Falkenstein et al., 2002; Fallgatter & Strik, 1999; Filipovic et al., 2000; Kok, 1986; Roberts, Rau, Lutzenberger, & Birbaumer, 1994; Shucard, McCabe, & Szymanski, 2008; Smith, Johnstone, & Barry, 2008). The No go-N2 and No go-P3 have traditionally been associated with inhibition control, which is a component of executive control and relates to the ability to deliberately suppress dominant and automatic proponent responses. However, recently several researchers (Botvinick et al., 2001; Bruin & Wijers, 2002; Bruin, Wijers, & van Staveren, 2001; Donkers & van Boxtel, 2004; Miller & Cohen, 2001; Troy et al., 2000; van Boxtel, van der Molen, Jennings, & Brunia, 2001; Yeung, Cohen, & Botvinick, 2004) have argued that the amplitude of No go-N2 mainly reflected the presence of conflict, and seemed to be unrelated to response inhibition, or at least related only to a limited extent. Response inhibition is one of the basic components of executive control functions. It is also possible that the No go-N2 and No go-P3 effects represent the sum of two intracranial generators. The first generator might be related to conflict and may originate from the medially located ACC (Braver, Barch, Gray, Molfese, & Snyder, 2001; Nieuwenhuis, Yeung, van den Wildenberg, & Ridderinkhof, 2003; Nieuwenhuis, Yeung, & Cohen, 2004), and the second generator with a more dorsolateral frontal location might reflect inhibition (Botvinick et al., 2001; Braver et al., 2001). In sum, researchers found two effects in No go stimuli when comparing them with Go stimuli in the visual Go/No go tasks. Firstly, there was a negative shift to the No go stimuli with the maximum at the frontocentral site with the latency of 150-400 ms being called the No go-N2. Secondly, a positive shift with the maximum at the frontal and central sites with the latency of 300-500 ms being the No-go-P3 (Falkenstein et al., 1999). Both subtly reflect changes in executive control functions. But in our study the amplitudes of N2 and P3 became smaller in the TSD group than in the NSD group because of the sleep deprivation.
The main purpose of this study was to verify whether or not executive control functions were impaired after 43 hours of total sleep deprivation (TSD), which would be reflected by the latencies and amplitudes of event-related potentials (ERP) components and behavioral data.
A total of 24 undergraduate students (mean age 19 [+ or -] 1.6 years, all male) were recruited from the Fourth Military Medical University and participated in the experiment for course credit. They were assigned randomly to either a total sleep deprivation (TSD) group or to a no sleep deprivation (NSD) group. All participants were right-handed and had normal or corrected-to-normal vision. None had previously participated in psychophysiological experiments. The general exclusion criteria were diseases of the central and peripheral nervous system, encephalic traumatisms, cardiovascular diseases and/or hypertension, cataracts and/or glaucoma, pulmonary problems, audiological problems, and alcohol and/or drug abuse. Participants were required to refrain from drinking alcohol, or eating or drinking food or beverages containing caffeine or chocolate for one week prior to, and also for the duration of, the study. The researchers assessed compliance with these instructions using sleep diaries and by calling participants the day before the beginning of the study. All participants had normal sleep patterns, defined as a typical bedtime of 9:30-10:00pm and a rising time of 6:00-7:00am. Additionally, on the Pittsburgh Sleep Quality Inventory, participants were tested and scored less than the clinical threshold of 5 (Buysse, Reynolds, Monk, Berman, & Kupfer, 1989), indicating that they were all good sleepers. In order to assess the presence of psychological conditions, participants completed the Symptom Checklist-90 (Derogatis, 1977), which indicates the frequency and intensity of 90 distress symptoms. None of the subjects had a T score on the General Symptom Index of more than 60 (the clinical range for symptoms in the general population involves T scores of over 63). Participants who completed both experimental sessions were paid an honorarium for their participation. This study was approved by the local ethics committee of the university, and all participants gave their written informed consent to participate after the experiments had been fully explained to them.
All participants completed a total of two experimental sessions. In the first session, they were familiarized with the visual Go/No go task and completed repeated trials of the task until their accuracy was consistently above 95%. In the second session in order to control their leisure and eating activities participants spent a total of three consecutive nights and four days in the laboratory. During the first two nights in the laboratory, participants were told to go to sleep at 9:30pm and wake up at 6:00am in order to familiarize them with the laboratory environment. During the third night, the TSD group was subjected to vigorous activities and had to stay awake. However, the NSD group was asked to go to sleep and to wake up at the same times as they had on the previous two (that is, 9:30pm and 6:00am). The experiment started at 6:00am on the morning of day two and ended at 9:00pm on day four. Participants in both groups were tested at 2:00am on the third day. During the period of TSD, all participants had no alcohol, caffeine, or chocolate, and were not allowed to have meals outside the prescribed meal schedule. Meals were served at 9:00am, 12:00pm, 5:30pm, and 10:00pm each day.
During the recording session, recording electrodes were fitted and participants were seated in a dimly lit, electrically shielded, and sound-attenuated cabin. Two white arrows pointing to the right or left were used as the stimuli, and were presented separately in the center of a black 19-inch screen, which was positioned so that the fixation point was in the center of the horizontal straight-ahead line of sight and placed 75cm away from the participants' eyes. Stimuli measured 2.0cm x 0.5cm (width 1.5[degrees], height 0.4[degrees]). Participants were instructed to press the right mouse button with the index finger of their right hand (dominant) when the stimulus arrows appeared. In each session, two experimental blocks were completed; each block consisted of 120 trials and lasted approximately 2.5 minutes. Each stimulus arrow was presented for 100 ms with an 800 ms interstimulus interval. The probability of occurrence of the target stimulus was 50%. The fixation mark was present on the screen whenever the stimulus disappeared. For one block, the arrow pointing to the right was the target stimulus, while for the other block, the response assignments were reversed so that the arrow pointing to the left was the target stimulus. Participants were allowed to rest for approximately 5 minutes between the two experimental blocks. The whole experiment, including placement of the electrodes and breaks, took approximately half an hour to complete. Participants were told to respond as quickly as possible while maintaining a high level of accuracy. The order of target stimuli and task blocks was counterbalanced across participants. Altogether, participants completed two blocks of the task, excluding the practice blocks.
Data Acquisition and Analysis
The electroencephalogram (EEG) was recorded using NeuroScan amplifiers on a 27-channel Easy cap with sintered Ag/AgCl-electrodes. Electrodes were placed according to the international 10-20 system. The ground and reference electrodes were placed near the left mastoid. Electrode impedance was kept below 5 k[ohms]. Four additional tin electrodes were attached for a bipolar recording of the vertical electrooculogram above and below the left eye and a horizontal electrooculogram was taken from the outer canthi of both eyes. Data were sampled at 1000 Hz and were amplified online with a high-pass frequency filter of 0.01 Hz and low-pass frequency filter of 100 Hz.
The continuous EEG was segmented off-line into epochs ranging from 100 ms prestimulus to 700 ms poststimulus and were baseline corrected to the mean amplitude of 100 ms before stimulus presentation. After the automatic artifact rejection, all trials were visually inspected and then rejected if eye movement artifacts or electrode drifts were visible. Ocular artifacts were estimated and subtracted by time domain regression analysis (Kenemans, Molenaar, Verbaten, & Slangen, 1991). All segments with a difference between minimum and maximum value exceeding 75 pV in any of the channels were automatically excluded from further processing. For each participant and each block, separate average ERPs were computed from the corrected data, for each stimulus category. Grand-averaged ERPs were displayed graphically for the purpose of identifying the major peaks. Peak detection was performed by means of a computer algorithm, which selects the time point in a specified latency window where a maximum or minimum voltage occurs. According to the grand-averaged ERPs, the latencies of each ERP component were detected in specified channels.
Analysis of ERP components was restricted to the sites F3, Fz, F4, C3, Cz, C4, P3, Pz, P4 in a 3 x 3 (lateral x sagittal) matrix. Peak and amplitude measures were subjected to a lateral (left/midline/right) x sagittal (frontal/central/parietal) x trial types (Go/No go) x groups (TSD group/NSD group) repeated measures multivariate analysis of variance (MANOVA). An analysis of variance (ANOVA) was performed for analysis of the behavioral data using groups as the factor. All posthoc tests were performed using the Bonferroni statistic. Statistical significance threshold was set at p < 0.05.
The mean correct reaction time (RT) data are presented in Table 1. Accuracy for both groups remained above 85%. The mean correct RT was significantly longer for the TSD group than for the NSD group which was mediated by a significant effect of group (F(1, 22) = 9.99, p < 0.05). The TSD group scored significantly more omission errors (misses) (F(1, 22) = 22.15, p < 0.01) and commission errors (false alarms) (F(1, 22) = 30.07, p < 0.01) compared to the NSD group.
ERP Peak Latencies
Figures 1 and 2 show the mean latencies of each ERP component in all the conditions. The group was the only factor that had a main significant effect on N1 latency (F(1, 22) = 99.54, p < 0.01). Similar main effects were also found for the latencies on P2 (F(1, 22) = 64.91, p < 0.01), N2 (F(1, 22) = 58.05, p < 0.01), and P3 (F(1, 22) = 16.02, p < 0.01). These effects could result from an increase in the latencies for the TSD group.
[FIGURE 1 OMITTED]
ERP Peak and Mean Amplitudes
As can be seen in Table 2 and Figure 2, the N1 showed a frontocentral topography, as revealed by main effects of lateral (F(2, 44) = 4.09, p < 0.01) and sagittal (F(2, 44) = 84.45, p < 0.01) sites on the N1 peak amplitude. There were also no differences in the N1 time window between groups. A main effect of trial types was, therefore, not found.
However, P2 showed a left parietal maximum, with effects of lateral (F(2, 44) = 5.13, p < 0.01) and sagittal areas (F(2, 44) = 48.56, p < 0.01) on P2 peak amplitude, and an interaction between them (F(4, 44) = 3.43, p < 0.01). The effect of trial types did not reach significance. A main effect of group (F(1, 22) = 3.84, p < 0.01) indicated that the amplitude of P2 was larger for the TSD than for the NSD group.
[FIGURE 2a OMITTED]
[FIGURE 2b OMITTED]
The No go-N2 was elicited reliably for all participants in all conditions. It was maximal at Fz and minimal at Pz, and was larger at Fz and Cz than was the Go-N2, and these results were confirmed by significant main effects of lateral (F(2, 44) = 8.02, p < 0.01), sagittal (F(2, 44) = 112.77, p < 0.01), and trial types (F(1, 22) = 37.00, p < 0.01). There were also significant differences between both groups in the peak amplitude of N2 (F(1, 22) = 5.00, p < 0.01). Moreover, the amplitude of No go-N2 was significantly lower for the TSD than for the NSD group.
The mean P3 amplitude reached its maximum at Cz, with an effect of sagittal sites (F(2, 44) = 7.44, p < 0.01), lateral sites (F(2, 44) = 3.46, p < 0.01) and the interaction between them (F(4, 44) = 2.90, p < 0.05). The P3 amplitude in No go trials was larger than that in the Go trials, which indicated a main effect of trial types (F(1, 22) = 3.46, p < 0.01). A main effect of group (F(1, 22) = 36.49, p < 0.01) was also found. Posthoc analysis showed that the mean No go-P3 amplitude for the TSD group was significantly smaller than that of the NSD group.
In this study, using a visual Go/No go task associated with activation of the executive control system, we examined whether or not 43 hours of total sleep deprivation has an influence on executive control functions.
Results indicated that executive control functions were noticeably impaired after 43 hours of TSD. It is, therefore, possible that the performance deterioration of the sleep-deprived participants could be related to an increase in their level of drowsiness (Chee & Chuah, 2008; Killgore et al., 2008; Lim & Dinges, 2008). However, the target stimuli were almost always accurately detected in all trials and very few false responses were made to the No go stimuli in our experiment. It is possible that the participants sacrificed speed in favor of being accurate, that is, they responded as quickly as they could without affecting their ability to maintain a high level of accuracy (Kopp, Rist, & Mattler, 1996).
Previous researchers (Alcaini, Giard, Thevenet, & Pernier, 1994; Naatanen & Picton, 1987; Natale, Marzi, Girelli, Pavone, & Pollmann, 2006) have found that N1 reflects sensory (or exogenous) processing, independent of cognitive activity. In our study, no differences were observed in N1 amplitude between the two groups, indicating that 43 hours of TSD did not affect the extraction of information from the early sensory analysis of simple visual stimuli. However, differences in the amplitude of P2 were found between the two groups. Lorenzo-Lopez et al. (2002) found that a larger P2 amplitude can indicate the existence of a deficit in the capacity to withdraw attentional resources from the stimulus in the task to which it is necessary to pay only marginal attention. The increase in the amplitude of P2 in the present study indicated that 43 hours of TSD contributed to the decrease in this capacity. Participants were informed that maintaining a high accuracy rate was important. Thus they needed to put in a certain amount of effort when performing the Go/No go task in order to maintain the higher levels of accuracy. It is worth noting that it may have been very difficult for the sleep-deprived participants to withdraw their attentional resources from the No go stimuli, which did not require any attention. The latencies of N1 and P2 were also significantly prolonged after 43 hours of TSD. These changes in the amplitudes and latencies of N1 and P2 represented a decrease in the capacity to allocate attentional resources efficiently during an early stage of processing after 43 hours of TSD.
In addition, there was a tendency for No go-N2 to be larger than Go-N2, which is consistent with the results of previous studies (Falkenstein et al., 1999; Falkenstein et al., 2002; Fallgatter & Strik, 1999, 2000; Kok, 1986; Oddy et al., 2005; Roberts et al., 1994; Ruchsow et al., 2008; Shucard et al., 2008; Smith et al., 2008). Falkenstein et al. (1999) found that the amplitude of No go-N2 was larger and the latency was shorter for good inhibitors as compared to poor. Recent findings have suggested that the amplitude and latency of No go-N2 reflects the effectiveness of inhibition responses or conflict detections, which is strongly related to performance (Botvinick et al., 2001; Bruin et al., 2001; Donkers & van Boxtel, 2004; van Boxtel et al., 2001; Yeung et al., 2004). In our study, the No go-N2 showed a frontocentral maximum consistent with distribution results from previous studies (Kopp, Mattler, Goertz, & Rist, 1996; van Veen & Carter, 2002). The decrease in the amplitude of the No go-N2 after 43 hours of TSD could be related to a reduction in the inhibition demands which are needed to prevent the execution of the anticipated Go response (Bruin et al.) or a decrease in response conflict evoked by the presentation of the No-go stimulus (Nieuwenhuis et al., 2003). In relation to this, the changes in No go-N2 indicated that the effectiveness of executive control functions was already significantly impaired after 43 hours of TSD.
The mean amplitude of No go-P3 indicated a frontocentral maximum, consistent the findings in several studies (Eimer, 1993; Falkenstein et al., 2002; Fallgatter and Strik, 1999; Kayser & Tenke, 2003; Roberts et al., 1994; Simson, Vaughan, & Ritter, 1977; Yeung et al., 2004). The amplitude of No go-P3 in the frontal region is related to the deployment of attentional resources (Praamstra & Seiss, 2005) and its latency reflects the time required for stimulus categorization and evaluation (Praamstra & Seiss, 2005; Ramautar, Kok, & Ridderinkhof, 2004). It has commonly been described as the marker of response inhibition. The sources of No go-P3 have been localized to a specific distribution network involving prefrontal, promotor and anterior cingulated areas (Weisbrod, Kiefer, Marzinzik, & Spitzer, 2000). In some studies it has been found that the No go-P3 amplitude varies as a function of stimulus probability and stimulus meaning, and could be reduced under conditions of uncertainty or low levels of confidence. Authors of previous studies have also reported that the No go-P3 amplitude decreases as its latency is prolonged during an extended period of wakefulness (Thomas et al., 2000). Along with increasing levels of uncertainty and difficulty in decision-making processes during sleep deprivation, the No go-P3 amplitude reduces and its latency is prolonged. In our study, the decrease in the No go-P3 amplitude was significantly reduced for the TSD group compared with that of the NSD group. This change, together with the increase in No go-P3 latency, reflected the fact that the capability of categorizing and evaluating a stimulus and the central capacity of identifying a target stimulus was significantly reduced for the sleep-deprived participants.
In summary, results in present study indicate that the amplitude of N2 was typically larger on No go trials than it was on Go trials with a very easy visual Go/No go task, for which there is considerable evidence of use of executive control functions. Executive control functions were significantly impaired after 43 hours of TSD, as evidenced by the amplitudes and latencies of ERP findings.
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General Air-Force Hospital, Beijing, People's Republic of China; The Fourth
Military Medical University, Xi'an, People's Republic of China, and Beijing
Institute of Basic Medical Sciences, Beijing, People's Republic of China
YONG-CONG SHAO AND DANMIN MIAO
The Fourth Military Medical University, People's Republic of China
MING FAN, GUO-HUA BI, AND ZHENG YANG
Beijing Institute of Basic Medical Sciences, Beijing, People's Republic of China
Jian-Lin Qi, General Air-Force Hospital, Beijing, People's Republic of China, The Fourth Military Medical University, Xi'an, People's Republic of China, and Beijing Institute of Basic Medical Sciences, Beijing, People's Republic of China; Yong-Cong Shao and Danmin Miao, The Fourth Military Medical University, Xi'an, People's Republic of China; Ming Fan, Guo-Hua Bi, and Zheng Yang, Beijing Institute of Basic Medical Sciences, Beijing, People's Republic of China. Appreciation is due to anonymous reviewers.
This study was supported by the Medical Sciences Foundation of the Chinese People's Liberation Army (06Z066). Jian-Lin Qi and Yong-Cong Shao contributed equally to the present paper. Special thanks to Shi-Jang Li, PhD, Professor of Biophysics at the Medical College of Wisconsin and Shihui Han, PhD, Professor of Psychology at Peking University. The authors also wish to thank Liping Fu and Jing Li.
Please address correspondence and reprint requests to: Danmin Miao, Department of Aerospace Psychology, The Fourth Military Medical University, Xi'an, Shannxi 710032, People's Republic of China. Phone: +86-10-68214026; Email: firstname.lastname@example.org or Zheng Yang, Beijing Institute of Basic Medical Sciences, Taiping Road 27, Beijing 100850, People's Republic of China. Phone: +86-10-68210161; Email: email@example.com
TABLE 1 Results of the visual Go/No Go Task for TsD and NsD groups Performance TSD group NSD group Mean correction RT in milliseconds (SD) 364 (43) * 335 (20) Misses rate (total) 13 ** 6 False alarm rate (total) 18 ** 7 Notes: TSD = total sleep deprivation; NSD = no sleep deprivation; RT = reaction time; Values are M (SD). * p < 0.05 and ** p < 0.01 compared to that for the NSD group. Table 2 Peak Amplitudes of Each ERP component during the visual Go/No Go task for TSD and NSD groups Amplitude (microvolts) NSD group Go No go N1 Fz -6.26 (3.90) -6.75 (2.28) Cz -5.53 (4.37) -7.31 (2.86) Pz -2.32 (4.54) -3.10 (2.50) P2 Fz 1.43 (5.04) -0.32 (3.65) Cz 1.38 (5.04) -0.87 (3.83) Pz 2.29 (4.09) 1.41 (2.15) N2 Fz -4.64 (5.42) -8.05 (4.06) Cz -2.50 (4.85) -6.67 (4.39) Pz -0.51 (4.22) -2.55 (4.13) P3 Fz 2.37 (3.40) 4.18 (2.32) Cz 3.52 (3.70) 4.30 (2.43) Pz 3.00 (3.10) 1.98 (1.82) Amplitude (microvolts) TSD group Go No go N1 Fz -6.70 (2.65) -7.09 (2.66) Cz -6.36 (3.64) -6.56 (2.61) Pz -3.19 (4.10) -2.75 (3.01) P2 Fz 3.03 (4.76) 0.61 (3.83) Cz 2.98 (5.32) -0.23 (3.75) Pz 3.80 (2.75) 2.46 (2.39) N2 Fz -4.09 (3.73) -6.31 (4.25) Cz -3.02 (3.92) -5.18 (3.93) Pz 0.30 (3.29) -1.29 (3.87) P3 Fz 1.53 (3.64) 2.37 (3.64) Cz 2.58 (2.87) 2.25 (3.05) Pz 2.89 (1.86) 2.25 (2.75) Note: TSD = total sleep deprivation; NSD = no sleep deprivation; values indicated are means, with standard deviations in parentheses. In the event-related potentials, peak amplitudes and latencies were taken from a time window of 50-150ms (N1, maximum negative peak), 250-350 ms (N2, maximum negative peak), 150-300ms (P2, maximum positive peak), and 300-500ms (P3, maximum positive peak). Additionally, 32 tin electrodes were arranged according to the International 10-20 system. In these electrodes, Fz reflects the frontocentral cortex, Cz the central cortex, and Pz the parietal lobe. Anterior cingulated cortex is commonly abbreviated to ACC.…
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Publication information: Article title: The Effects of 43 Hours of Sleep Deprivation on Executive Control Functions: Event-Related Potentials in a Visual Go/no Go Task. Contributors: Qi, Jian-Lin - Author, Shao, Yong-Cong - Author, Miao, Danmin - Author, Fan, Ming - Author, Bi, Guo-Hua - Author, Yang, Zheng - Author. Journal title: Social Behavior and Personality: an international journal. Volume: 38. Issue: 1 Publication date: February 2010. Page number: 29+. © 2009 Scientific Journal Publishers, Ltd. COPYRIGHT 2010 Gale Group.
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