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1 Respiratory Medicine Unit and 2 Department of Medical Physics, The University of Edinburgh, Royal Infirmary, Edinburgh EH3 9YW, Scotland, United Kingdom
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The prevalence of irregular breathing during sleep
is age and gender dependent, but the reason for this is unknown. This study tested the hypothesis that older men have a greater sleep-related increase in respiratory resistance. In 48 healthy subjects, 12 in each
of four groups of younger and older men and women, airway resistance
was measured during wakefulness and sleep using a mask, pneumotachograph, and catheter-mounted pressure sensors. Total respiratory resistance and total "low-flow," and "high-flow"
oropharyngeal resistance were analyzed from 170,000 breaths, high flow
being at rates above 50% maximal inspiratory flow. High-flow
oropharyngeal and total respiratory resistance increased during
non-rapid eye movement (NREM) sleep in all groups but not low-flow
resistance. Total respiratory resistance increased from 12 ± 1.2 cmH2O · l
1 · s1
awake to 16.2 ± 2.4 in NREM sleep in young men, from 22.8 ± 3.6 to 33.6 ± 5.4 in young women, from 18 ± 3 to 34.8 ± 4.8 in older men, and from 26.6. ± 4.2 to 34.2 ± 6 in older
women. The percentage of change in total respiratory resistance from
awake to NREM sleep was not different between age groups or genders. We
conclude that there are no major age or gender differences in the
changes in airway resistance with sleep in normal subjects.
prevalence; sleep apnea/hypopnea syndrome; pharynx; rapid eye movement
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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IN NORMAL SUBJECTS, THE PREVALENCE of irregular breathing during sleep is higher in men than in women and also higher in the middle-aged than in the young (2). Similarly, the prevalence of the sleep apnea/hypopnea syndrome is both age and gender dependent (32), affecting ~2% of middle-aged women and 4% of middle-aged men (43). However, the reasons that age and gender affect breathing during sleep are not clear.
Many studies in awake subjects have tried to elucidate the reasons for the gender difference in breathing during sleep. These have found that men have larger upper airways when awake and sitting (4, 26) but greater collapsibility of the upper airway with changes in lung volume (4) or posture (26). Increasing age results in decreasing upper airway size in awake men (6, 26, 41) and women (26). However, there have been few studies examining the interaction of sleep with age and gender on upper airway caliber. One recent study found a greater increase in upper airway resistance in stage 2 sleep in young men compared with young women (38). An investigation of breathing pattern and upper airway mechanics in sleep showed greater oscillations in upper airway resistance in older than in younger individuals, but there have been no comparative studies during overnight studies and all sleep stages. We have, therefore, tested the hypothesis that middle-aged men would narrow their upper airways more during sleep than women or younger men.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects
Volunteers were recruited from the general population of Edinburgh by a newspaper advertisement not referring to sleep. All gave written, informed consent to participate in the study, which had the approval of the local ethical advisory committee. Subjects took no medication or alcohol on the day of study. Responding volunteers were sent a questionnaire providing information about lifestyle, sleeping habits, snoring, and daytime function. Subjects were grouped according to gender and age, the younger group ranging from 18 to 35 years, the older group from 40 to 70 years. All body mass indexes were below 30 kg/m2. All denied sleep complaints, excessive daytime sleepiness (Epworth Sleepiness Scale
10), were non- or only
very occasional snorers, had no witnessed apneas (confirmed by the bed
partner), and were free from respiratory or cardiovascular disease.
Height, weight, and neck circumference measured at the
cricothyroid membrane were recorded (Table
1). Subjects reported to the laboratory
2-3 h before bedtime for setup. They were encouraged to sleep in
their usual sleeping body positions, except that lying prone was not possible because of the face mask. Participants were not sleep deprived, and no acclimatization studies were done.
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To achieve the 12 patients in each group, as was determined a priori, 52 subjects were recruited. One subject was excluded because she did not enter rapid eye movement (REM) sleep and one because of a total sleep time of only 90 min. The remaining two were excluded because of technical failure.
Upper Airway Dimensions
Upper airway dimensions in the awake state were measured using the acoustic-reflection technique (13, 21). The system used in this study was adapted by Marshall and colleagues (25) and validated with airway models, human volunteers, and magnetic resonance imaging scanning (22, 24). In human volunteers, the within-run coefficient of variation for acoustic-reflection measurement is 10%, similar to that found by Brooks et al. (3). Measures were performed in awake subjects in the sitting and supine positions.Four upper airway measurements were read off the mean trace (26): oropharyngeal junction (OPJ; cm2); maximum pharyngeal area (cm2), mean cross-sectional area from the OPJ to the glottis (cm2), and pharyngeal volume (cm3) as the integrated area under the curve between the OPJ and the glottis.
Polysomnography
All subjects underwent a night of full polysomnography (PSG, Compumedics) using standard techniques (12). Measurements included central and frontal electroencephalograms (EEG,C3-C4, CZ-PZ, F3-FP1, F4-FP2), two electrooculograms (EOG), and submental electromyograms (EMG). Nasal airflow was taken from a tightly fitting nose mask with a soft silastic seal (ResMed UK, Oxford, UK), to which a pneumotachograph (F100L, gm instruments, Kilwinning, UK, Resistance 0.44 cmH2O · l1 · s1
at 1 l/s, linear range ± 100 l/min), connected to a differential pressure transducer (Furness controls, FC014, Bexhill, UK) was attached. This system had a dead space of ~65 ml, depending on the
subject's face configuration. The pneumotachograph was calibrated with
a rotameter before each procedure. Linearity of the flow signal was
demonstrated over the range of interest (±0.5 l/s). EEG and airflow
data were sampled at frequencies of 125 and 50 Hz, respectively, and
pressures at 25 Hz. No subject complained of discomfort with the mask
in place. The system was tested airtight to a negative pressure of 
30
cmH2O. Oropharyngeal and esophageal differential pressure
swings were measured with a solid-state two-pressure-sensor transducer
custom built into a single catheter (Gaeltec, Skye, Scotland; external
diameter 2.4 mm; resistive strain gauges, temperature coefficient of
sensitivity < 0.2%/C°), with reference to the mask pressure.
The sensors were calibrated at 37° in a water column before each
recording. The catheter was placed transnasally under topical
anesthesia (one puff of lidocaine 10% to the nostril and one puff to
the oropharynx), into the esophagus (typically 35 cm from the nares),
the oropharyngeal sensor under visual control just below the uvula, the
correct position being confirmed in the supine posture. The pressure
transducer was secured at the tip of the nose, placed in juxtaposition
to the face, and led out underneath the mask. To ensure that any effect
of the topical anesthesia was gone before data collection, the catheter was placed first so that a minimum of 30 min passed before lights out.
Oral airflow was detected by a thermistor taped in place in front of the lips. All breaths with visually detectable oral airflow were excluded from the analysis. Resistances for the awake state were taken only from the 5 min before the first sleep period and in wake periods thereafter. Thoracoabdominal movement was recorded by inductance plethysmography and oxygen saturation by pulse oximetry (Ohmeda, Essex, UK). Snoring was detected from a microphone attached to the head of the bed.
Definition of Nocturnal Events
Apnea was defined as the cessation of nasal airflow for at least 10 s. Hypopnea was defined as more than a 50% decrease in the nasal tidal volume for at least 10 s (1, 14). Type of apnea (obstructive, mixed, or central) was defined according to the pattern of esophageal pressure swings throughout the event (11). Arousals were defined as a return of alpha or theta rhythm for at least 1.5 s with an associated transient EMG rise (8).Analysis
Breaths with obvious artifacts such as swallowing, mouth breathing, or coinciding arousal with increase in muscle tone were visually identified and discarded. All remaining breaths were analyzed automatically by self-written computer software. Inspiratory resistance was calculated breath by breath as steepness of the least square regression of the entire inspiratory pressure-flow relationship. On average, the inspiratory pressure-flow relationship was characterized by >50 distinct samples per inspiration for calculation of the regression relationship.The pressure-flow relationship was not always linear in sleep with
flattening of the relationship at higher pressures. To allow analysis
of these flow-limited breaths, the inspiratory flow curve for all
breaths was arbitrarily partitioned at 50% of the maximal flow into
two sections for which two least square pressure-flow regression lines
were calculated. The relationships obtained in the first (low-flow)
section were given the suffix "1" and those in the second
(high-flow) section the suffix "2." The flow-time profile and
inspiratory resistance at the oropharynx of an unobstructed breath are
given in Fig. 1. An example of a breath
in which high-flow inspiratory resistance is markedly different from
low-flow resistance is given in Fig. 2.
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Mean resistance was calculated for each subject for awake and each sleep stages. We used the definitions for the anatomical segments of the upper airway as proposed by Shepard and Thawley (37). For total respiratory resistance (RL), pressure swings were measured at the esophagus; for resistance of the nose, nasopharynx across the soft palate, pressure swings were measured at the oropharynx (Roro). The difference between resistance measured at the esophageal and the oropharyngeal levels represents the gradient across the lungs, larynx, and supralaryngeal airway up to the oropharynx. For measuring RL between awake and the first sleep onset, the two epochs of 30 s closest to the transition from alpha to theta EEG activity were taken for analysis.
For each group, mean ± SE values for the results of functional evaluation were calculated. Absolute values of resistance within individuals were taken for comparisons between groups. Analysis of variance (ANOVA) was used with categorization by sleep state and age and gender group as well as for comparisons within the same group. This was followed by the Newman-Keuls multiple comparisons procedure, where appropriate. Statistical significance is taken at P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects and Sleep Data
Subjects were similar in body mass index and Epworth sleepiness scale (23). There were only minor differences in basic sleep parameters between groups (Table 1). Women and younger men had a significantly lower apnea/hypopnea index than older men. Men had bigger neck circumferences and waist-to-hip ratios than women.Mean recording time was 391 ± 4 min. The overall sleep efficiency was 66 ± 2%. All 48 subjects entered stage 4 and REM sleep. After excluding breaths with any mouth breathing or obvious artifacts, a total of 45,413 breaths were analyzed in the awake state and 123,944 breaths in sleep (Table 1).
Effect of Age and Gender on Upper Airway Dimensions When Awake
The acoustic reflection studies showed that younger women had narrower upper airways at all sites than the younger men in both sitting and supine positions. The younger women also had narrower OPJs and smaller mean pharyngeal cross-sectional areas than the older men and women (Table 2).
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Effect of Age and Gender on Upper Airway Resistance During Total Sleep
Changes within groups.
Oropharyngeal resistance at low flow rates (Roro1) did not
increase significantly from awake to either non-rapid eye movement (NREM) or REM sleep in any group (Table
3). All groups demonstrated a higher Roro
in the second (Roro2; Fig. 3)
than in the first section of the pressure-flow relationship when awake
and also in both NREM and REM sleep (Table 3). In all groups,
Roro2 increased significantly between awake and NREM sleep,
but only in the older men was Roro2 significantly higher in
REM sleep than in wakefulness (Table 3). RL increased
significantly between waking and NREM sleep in all four groups.
RL increased significantly from waking to REM sleep in the
younger women and older men only.
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Differences between groups. There was no significant differences between groups in the percentage change in initial Roro (Roro1) from wakefulness to either NREM or REM sleep. There was a greater percentage increase in Roro2 between awake and NREM sleep in young women than in young men, but the percentage changes between waking and REM sleep did not differ between groups.
The increases (%) in RL between the awake state and NREM sleep did not differ in the four groups.Effect of Age and Gender on Changes in Airways Resistance at Sleep Onset
At the transition from waking to sleep, there were significant increases in RL in the younger and older men but not in women. However, there were no significant differences between subject groups in the RL changes at sleep transition (Table 4). There were no significant differences between groups in either Roro1 or Roro2 at sleep onset.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This study shows that there were no major differences between the genders or with age in the changes in airway resistance from wakefulness to stable sleep in healthy subjects. There was no change between waking and sleep in Roro at lower flow rates, but both Roro at high flow rates and total respiratory resistance increased during both NREM and REM sleep compared with wakefulness, suggesting some degree of upper airway collapsibility. At the transitions from wakefulness to NREM sleep, there were significant increases in total respiratory resistance in men only.
There is no gold standard method of expressing respiratory resistance over the entire respiratory cycle. This is reflected by the many different ways researchers in this field have dealt with this problem. In most investigations, resistance is calculated at maximum pressure swings (40), as pressure deflection at a constant flow rate (41), at midinspiration (31), or at maximal flow. Calculating resistance by portioning the breath into equal sections (30) was first employed by Henke et al. (17); another group divided the inspiratory signal into 11 equal portions and averaged the middle 7 to produce a RL inspiratory value for that breath (29). Weaknesses of these approaches become most apparent as soon as flow limitation occurs, because the pressure-flow relationship is no longer linear beyond the occurrence of flow limitation. The pressure-flow relationship may be described by the Rohrer equation (36) in this situation. However, Hudgel et al. (20) observed that the inspiratory pressure-flow relationship of the upper airways in healthy subjects was often too curvilinear even to be predicted by the Rohrer equation, requiring more complicated curve-fitting models. This complex polynomial approach could have been used in the current study. However, we think our approach is valid, clear, and more generally understandable and also allows numerical analysis of group data.
Recently, inspiratory flow limitation in snorers has been assessed by looking at changes in flow rate for a minimal pharyngeal pressure reduction. Breaths were divided into categories (levels 1-4), using the "shape" of the flow-time profile and applying mathematical curve-fitting models, which was possible only for "mild" (level 2 of four distinct levels) flow limitation (9). Hence, no continuous characteristics of flow limitation are available so far. Efforts have been made to determine the proportion of flow-limited breaths in patients with the obstructive sleep apnea syndrome and the upper airway resistance syndrome (10, 15). However, no data about the frequency of occurrence and impact of flow-limited breaths in the healthy, nonsnoring population have been available so far. In our study, we opted for the combination of a simple approach to calculate resistance; a least square regression line of the entire inspiratory pressure-flow relationship as proposed by Mead and Whittenberger (27) also divided the inspiratory flow curve into two segments at an arbitrarily chosen 50% of the maximal flow to allow separate examination of inspiratory flow limitation. The higher 50% demonstrated a consistently higher resistance than the lower 50% of the flow swing in all groups and also a significant increase from wakefulness to NREM sleep but not to REM sleep. This suggests a higher degree of flow limitation occurring in NREM than in REM sleep. This could be due to decreased upper airway collapsibility in REM sleep, although lower flow rates associated with the hypoventilation found in REM sleep would be another possible explanation (13).
Various sites along the upper airway are prone to narrow and collapse in patients with obstructive sleep apnea during sleep (7, 18, 33). In almost all sleep apnea/hypopnea subjects, the segment that narrowed maximally was above the oropharyngeal segment investigated in these studies (7, 19). Using pressure recordings at the oropharynx, just below the uvula, and in the esophagus enabled us to look for distinct age- and gender-related patterns of airway obstruction at these sites. We were unable to identify age- and gender-related differences in airway resistances at either level irrespective of sleep stage. Moreover, significant differences in upper airway dimensions between groups did not correlate with changes of airway resistance between awake and asleep. Our absolute values of upper airway resistance compared with some other studies appear high, especially in the group of younger women. Due to our random selection of study subjects allocated by a newspaper advertisement, we are not aware of any anatomical or ethnic component. Using a nose mask instead of a full face mask could have had some effect on nose resistance, although we carefully looked to avoid any compression of soft parts of the nose. Supposedly, our pressure transducer did not interfere more with nose patency than did pressure transducers used in other investigations. Our resistance measurements were made with the subjects lying down, which will increase resistance compared with studies in which measurements were made in seated subjects (22).
The results from our study are in contrast to those in a previous investigation. Trinder et al. (38), in a similar number of young participants, showed a greater increase in upper airway resistance during NREM sleep in healthy young men than in women. However, the main focus of that study was obtaining data at sleep transitions by repeatedly awakening the subjects after they had been sleeping for 5-10 min and then restudying them as they went to sleep again. Thus Trinder's subjects experienced sleep fragmentation, which may have altered their upper airway muscle tone (39) in comparison with our subjects. Another difference was that Trinder and colleagues used a full face mask with a dead space of 155 ml as opposed to our 65-ml dead space nose mask system, and they also measured oropharyngeal pressure ~1 cm below the level in the current study. Furthermore, their young women and men had similar resistances when awake, whereas our young women had higher resistances. We believe that our finding of higher resistances during wakefulness in women was correct because it is corroborated by an independent technique, acoustic reflection, which showed that women had narrower upper airways when awake, and by previous studies (4, 26). Another difference was that Trinder's subjects were marginally younger (mean age 20 yr) than our young group (26 yr). In addition, Trinder reported his data as the resistance at peak flow. Because men have higher levels of ventilation than women, this could result in higher resistances at peak flow merely by the men having higher peak flows on the same alinear pressure-flow relationship. Thus there are various methodological differences that may explain some of the differences between Trinder's study and the present one. Our sleep transition data showed significant increases in resistance in the men but not in the women. If this finding is substantiated, this phenomenon could contribute to the higher frequency of obstructive apneas and hypopneas found in men because these tend to occur at sleep transitions. It is remarkable that, although ventilation has been shown to decrease at sleep onset, upper airway resistance increases, possibly as a result of a reduction in activity of upper airway dilating muscles with sleep (42).
This study is based on analysis of almost 170,000 breaths, with an average of over 3,000 breaths per subject. The large number of breaths, when combined with the high sampling rate and an average of >50 samples per breath, increases reliability of the findings of this study. However, potential weaknesses include between-subject variation, the effects of the instrumentation on the measurements made, and multiple end points. The variance in baseline resistances in both wakefulness and sleep can be seen from the tables and figures. As seen best in the figures, most subjects showed changes that were consistent with the other subjects in that group, but in most groups there were one or more subjects who responded differently. We could not identify any differences in the characteristics of the subjects who reacted in this way, and so this may have been due to random chance alone, but more studies would be needed to be certain. However, this study already represents a large data set of all-night data from 48 normal subjects. The sleep quality observed was fair for the degree of instrumentation. The increased airflow resistance caused by the catheter is unavoidable if resistance is to be measured and partitioned, but the catheter used was fine (external diameter 2.4 mm) and contained both the oropharyngeal and esophageal pressure-sampling systems. The catheter used had a "side-viewing" pressure transducer to minimize artifacts due to the momentum of airflow. This represents a significant advantage over the use of balloons or catheter end sensors.
A statistical problem with the study is that it had 144 end points, namely the difference in resistance with age and gender between sleep states, both during consolidated sleep and at transitions and the intergroup comparisons. On this basis, seven (144/20) end points would be expected to be significant merely by chance alone when significance is assessed at the 5% level. We found 49 significant differences, and thus we believe most are likely to be genuine rather than chance associations.
Upper airway patency is determined in part by the difference between intraluminal and extraluminal pressure and the stiffness of the upper airway. This stiffness is largely determined by upper airway muscle activity. It is generally assumed that changes in upper airway muscle activity are a major factor contributing to sleep-induced changes in upper airway resistance. When awake, sleep apnea patients have significantly greater basal genioglossal activity compared with controls (28). It has been proposed that the loss of wakefulness is associated with a reduction in activity of the upper airway-dilating muscles (5, 35). However, there is also evidence that elastic elements of the airway wall, depending, for example, on the amount and characteristics of connective tissue, influence pharyngeal compliance (34). Therefore, the observed differences in upper airway resistance between awake and different sleep stages might reflect an age- and gender-related difference in activity of these muscles or differences in elastic tissue properties of the pharynx.
It has been suggested that young healthy nonobese people are not dependent on phasic upper airway muscle activity to maintain airway patency during sleep, at least when nonsnoring (16). Hence, tonic muscle activity and upper airway structure alone may keep the upper airway open in healthy young people. This might apply also for older people and both genders, at least in part explaining the lack of differences in upper airway resistance responses to sleep in different age and gender groups. On the other hand, it has also been shown that phasic palatal muscle EMG responses to negative pressure in awake sleep-apneic patients is altered compared with healthy subjects (30). Therefore, perhaps, patients with sleep apnea/hypopnea syndrome may have both impaired tonic and phasic activity of upper airway muscles contributing to an increased pharyngeal compliance. However, the reason why men in the middle-aged group should be more prone to suffer a loss of tonic and phasic muscle activity remains to be explained. The fact that the initial oropharyngeal resistance (Roro1) does not vary between wakefulness and sleep suggests that there is no major change in airway caliber at low flow rates between sleep stages. In contrast, the significant increases in resistance at higher flow rates (Roro2) suggest dynamic changes in airway collapsibility between sleep stages. Age- and gender-related differences in the collapsibility of the upper airway need investigation.
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ACKNOWLEDGEMENTS |
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We thank the night nursing staff and technicians of the Sleep Center for their help and Dr. G. B. Drummond, Department of Clinical and Surgical Sciences, The University of Edinburgh, for technical support.
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FOOTNOTES |
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R. Thurnheer was supported by a grant from the Swiss National Science Foundation (Stipendium für angehende Forscher der Forschungskommission des Schweizerischen Nationalfonds; 81 ZH-049909) and the Schweizerische Gesellschaft für Pneumologie.
Address for reprint requests and other correspondence: N. J. Douglas, Respiratory Medicine Unit, Univ. of Edinburgh, Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW, Scotland, UK (E-mail: njd{at}srv1.med.ed.ac.uk).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 7 March 2000; accepted in final form 4 October 2000.
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TOP
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METHODS
RESULTS
DISCUSSION
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