human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVE To study morphometric and qualitative histopathologic changes of the soft palate and uvula in patients with mild , moderate , and severe obstructive sleep apnea . STUDY DESIGN A prospect i ve , nonr and omized controlled study . METHODS The distal soft palate and uvula were excised during uvulopalatopharyngoplasty from 34 male patients with obstructive sleep apnea . Control  specimens were retrieved from 7 male cadavers with no related disorders . All specimens underwent routine processing and the mid-sagittal sections were studied . Morphometric analysis of the relative proportions of the tissue constituents was carried out . Also , a qualitative assessment was performed to detect possible pathologic changes . RESULTS The body mass index of patients was significantly higher from that of control subjects . The area fraction occupied by the tissue constituents of the distal portion of the soft palate and uvula in patients with mild , moderate , and severe obstructive sleep apnea and in control subjects was similar , with small and insignificant differences regarding the contents of gl and s , muscle , fat , blood vessels , and the epithelium . Only the connective tissue was significantly greater in patients with moderate obstructive sleep apnea than in those with severe obstructive sleep apnea and control subjects . The qualitative assessment of the specimens disclosed normal tissue architecture without evidence of destruction . Vascular engorgement , fibrosis , edema , inflammatory cell infiltration , and dilated gl and ular ducts were observed in a portion of patients and control subjects . CONCLUSIONS The structure of the distal soft palate and uvula of patients with obstructive sleep apnea undergoes insignificant changes and is independent of the body mass index levels , indicating that the pathologic changes are probably the sequela of airway obstruction rather than its cause HYPOTHESIS The pathophysiology of snoring and obstructive sleep apnoea is still unclear . Two theories are proposed . The first is the obstructive theory , which postulates palatopharyngeal muscle hypertrophy leading to airway narrowing ; there is no neural role . The second is the neurogenic theory , which postulates neural degeneration due to vibratory stretch trauma , leading to muscle atrophy and collapse . As identification of nerve fibres in the uvula and palate is difficult and time-consuming , all previous studies aim ing to differentiate between these two theories have been based on indirect observation of the muscles , rather than direct study of the nerves . METHODS We conducted a prospect i ve study to directly observe and study nerve fibres in uvular specimens from 10 cases of obstructive sleep apnoea , compared with specimens from 10 cases of simple snoring , using transmission electron microscopy .  Five autopsy cases served as controls . RESULTS Obstructive sleep apnoea was associated with definite degenerative changes in myelinated and unmyelinated nerve endings . These degenerative changes were present to a lesser degree and in a smaller proportion of cases of simple snoring . CONCLUSION The events postulated by the neurogenic theory of obstructive sleep apnoea appear to play an important role in the pathophysiology of snoring and obstructive sleep apnoea Sleep-disordered breathing is a common disorder with a range of harmful sequelae . Obesity is a strong causal factor for sleep-disordered breathing , and because of the ongoing obesity epidemic , previous estimates of sleep-disordered breathing prevalence require updating . We estimated the prevalence of sleep-disordered breathing in the United States for the periods of 1988 - 1994 and 2007 - 2010 using data from the Wisconsin Sleep Cohort Study , an ongoing community-based study that was established in 1988 with participants r and omly selected from an employed population of Wisconsin adults . A total of 1,520 participants who were 30 - 70 years of age had baseline polysomnography studies to assess the presence of sleep-disordered breathing . Participants were invited for repeat studies at 4-year intervals . The prevalence of sleep-disordered breathing was modeled as a function of age , sex , and body mass index , and estimates were extrapolated to US body mass index distributions estimated using data from the National Health and Nutrition Examination Survey . The current prevalence estimates of moderate to severe sleep-disordered breathing ( apnea-hypopnea index , measured as events/hour , ≥15 ) are 10 % ( 95 % confidence interval ( CI ) : 7 , 12 ) among 30 - 49-year-old men ; 17 % ( 95 % CI : 15 , 21 ) among 50 - 70-year-old men ; 3 % ( 95 % CI : 2 , 4 ) among 30 - 49-year-old women ; and 9 % ( 95 % CI : 7 , 11 ) among 50 - 70 year-old women . These estimated prevalence rates represent substantial increases over the last 2 decades ( relative increases of between 14 % and 55 % depending on the subgroup ) It has previously been reported that the duration of  obstructive apneas  increases from the beginning to the end of the night ( M. Charbonneau , J. M. Marin , A. Olha , R. J. Kimoff , R. D. Levy , and M. Cosio . Chest 106 : 1695 - 1701 , 1994 ) . The purpose of this study was to test the hypothesis that stimulation of upper airway ( UA ) sensory receptors during obstructed inspiratory efforts contributes to arousal and apnea termination and that a progressive attenuation of this mechanism through the night contributes to apnea lengthening . We studied seven patients ( six men , one woman ) with severe obstructive sleep apnea ( apnea-hypopnea index = 93 + /- 26 events/h ) during two consecutive nights of polysomnographic monitoring .  On one night ( r and om order ) , we performed topical UA anesthesia with 0.2 % tetracaine and on the control night , sham anesthesia . We measured apnea duration , esophageal pressure ( Pes ) during apneas , and apneic O2 desaturation . Consistent with previous findings , apnea duration , number of efforts per apnea , and peak Pes at end apnea increased from the beginning to the end of the control nights . UA anesthesia produced a significant increase in apnea duration at the beginning of the night but no change in apnea length at the end of the night . Peak Pes and the rate of increase in Pes during the anesthesia nights were greater than during control nights , but the rate of increase in Pes was similar for the beginning and end of the control and anesthesia nights . These findings suggest that UA sensory receptors play a role in mediating apnea termination at the beginning of the night but that the contribution of these receptors diminishes as the night progresses such that greater inspiratory efforts are required to trigger arousal , leading to apnea prolongation This study was conducted to determine whether inflammation is present in the uvula mucosa of patients with obstructive sleep apnea ( OSA ) . Uvulas were obtained by uvulopalatopharyngoplasty in 21 patients with moderate OSA ( mean apnea/hypopnea index and st and ard error of the mean : 32 + /- 4 ) and by  autopsy in 5 individuals not known to have OSA . Using point counting in five r and omly selected high-power microscopic fields ( X100 ) , the authors found that the number of leukocytes in the lamina propria of the uvula mucosa was significantly higher in patients with OSA than in the controls ( 179 + /- 12 cells vs. 71 + /- 4 cells , respectively ; P < .05 ) . This was due to a significant increase in the number of plasma cells in patients with OSA as compared with controls ( 89 + /- 15 cells vs. 21 + /- 5 cells , respectively ; P < .05 ) . The thickness of the lamina propria ( an index of interstitial edema ) was also significantly increased in patients with OSA compared with controls ( 0.99 + /- 0.12 mm vs. 0.27 + /- 0.02 mm , respectively ; P < 0.05 ) . The authors conclude that inflammation , characterized by plasma cell infiltration and interstitial edema , is present in the uvula mucosa of patients with moderate OSA . They also suggest that soft palate inflammation contributes to upper airway occlusion observed during sleep in these patients Previous studies support the presence of an upper airway reflex mechanism that contributes to the maintenance of upper airway patency during sleep . We investigated the possibility that interference with this reflex mechanism contributes to the development of  obstructive sleep apnea . Eight otherwise asymptomatic snorers ( seven male and one female ) , age 39 + /- 5.3 yr ( mean + /- SEM ) , underwent overnight sleep studies on three successive nights . An acclimatization night was followed by two study nights r and omly assigned to control ( C ) and oropharyngeal anesthesia ( OPA ) . On the OPA night topical anesthesia was induced using 10 % lidocaine spray and 0.25 % bupivacaine gargle . A saline placebo was used on night C. All subjects slept well on both study nights ( mean sleep duration was 6.2 h on both study nights ) , and sleep stage distribution was similar on both nights . Obstructive apneas and hypopneas ( OAH ) rose from 114 + /- 43 during C to 170 + /- 49 during OPA ( p less than 0.02 ) . Central apneas and hypopneas ( CAH ) were unchanged between the two nights ( 8 + /- 4.9 versus 7 + /- 3 ) . The duration of OAH was similar on both study nights ( 20 + /- 1.9 s during C versus 20 + /- 1.5 s during OPA ) . The frequency of movement arousals terminating OAH tended to be higher during OPA ( 7 + /- 2.9/h ) than during C ( 3 + /- 0.7 ) ; P = NS . The frequency of oxyhemoglobin desaturations was also higher during OPA ( 5 + /- 2.1/h ) than during C ( 3 + /- 1.4 ) , p less than 0.07 . ( ABSTRACT TRUNCATED AT 250 WORDS Previous studies indicate that upper airway ( UA ) sensory receptors play a role in the maintenance of UA patency and contribute to arousal in response to airway occlusion . An impairment of UA sensory function could therefore predispose to UA obstruction during sleep . We hypothesized that UA sensation is impaired in obstructive sleep apnea ( OSA ) , and that sensation improves after treatment with nasal continuous positive airway pressure ( CPAP ) . We measured two-point discrimination ( 2PD ) and vibratory sensation thresholds ( VT ) in 37 patients with OSA ( mean [ + /- SE ] apnea- hypopnea index [ AHI ] = 39 + /- 5 events/h ) , 12 nonapneic snorers ( SN ) , and 15 control subjects ( CL ) . Sensory thresholds were determined in the UA and on the lip and h and as control sites . Both 2PD and VT were similar among the three groups at the lip and h and sites but were significantly reduced in the UA of OSA and SN subjects versus CL ( p < 0.05 ) . Values for 2PD and VT in the UA of OSA versus SN were not significantly different . Sensory measures were repeated after 6 mo in 23 OSA patients treated with CPAP as well as in 18 untreated patients . Thresholds for 2PD and VT at control sites remained identical in both groups , as did 2PD for the UA . However , VT in the UA showed a significant improvement in treated ( 4.4 + /- 0.2 pre-CPAP versus 3.8 + /- 0.2 mm post-CPAP , p < 0.05 ) but not untreated patients . These findings indicate the presence of a selective impairment in the detection of mechanical stimuli in the UA of patients with OSA and SN , which is partially reversible after treatment with nasal CPAP in patients with OSA Snoring is a very common problem but there are few publications on the histological findings of the soft palate/uvula and these lack consistency . The relative proportions of tissue types in the base of the uvula removed from 17 adults who underwent uvulopalatopharyngoplasty for heavy snoring were therefore compared with 14 cadaveric specimens . The mean percentage of muscle from the snoring group was 12.1 % compared with 7.2 % in the control group ( P < 0.05 ) . The percentage of fibrous tissue was greater in the cadavers ( 52.8 % vs 45.5 % in the snorers , P < 0.05 ) . The percentage of muscle was inversely related to the percentage of fibrous tissue in the snoring group ( P < 0.02 ) . We hypothesize that these changes are a consequence of the repetitive forces on the soft palate during snoring rather than being related to the pathogenesis of snoring 
    Output:
    
agent
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVE To study morphometric and qualitative histopathologic changes of the soft palate and uvula in patients with mild , moderate , and severe obstructive sleep apnea . STUDY DESIGN A prospect i ve , nonr and omized controlled study . METHODS The distal soft palate and uvula were excised during uvulopalatopharyngoplasty from 34 male patients with obstructive sleep apnea . Control  specimens were retrieved from 7 male cadavers with no related disorders . All specimens underwent routine processing and the mid-sagittal sections were studied . Morphometric analysis of the relative proportions of the tissue constituents was carried out . Also , a qualitative assessment was performed to detect possible pathologic changes . RESULTS The body mass index of patients was significantly higher from that of control subjects . The area fraction occupied by the tissue constituents of the distal portion of the soft palate and uvula in patients with mild , moderate , and severe obstructive sleep apnea and in control subjects was similar , with small and insignificant differences regarding the contents of gl and s , muscle , fat , blood vessels , and the epithelium . Only the connective tissue was significantly greater in patients with moderate obstructive sleep apnea than in those with severe obstructive sleep apnea and control subjects . The qualitative assessment of the specimens disclosed normal tissue architecture without evidence of destruction . Vascular engorgement , fibrosis , edema , inflammatory cell infiltration , and dilated gl and ular ducts were observed in a portion of patients and control subjects . CONCLUSIONS The structure of the distal soft palate and uvula of patients with obstructive sleep apnea undergoes insignificant changes and is independent of the body mass index levels , indicating that the pathologic changes are probably the sequela of airway obstruction rather than its cause HYPOTHESIS The pathophysiology of snoring and obstructive sleep apnoea is still unclear . Two theories are proposed . The first is the obstructive theory , which postulates palatopharyngeal muscle hypertrophy leading to airway narrowing ; there is no neural role . The second is the neurogenic theory , which postulates neural degeneration due to vibratory stretch trauma , leading to muscle atrophy and collapse . As identification of nerve fibres in the uvula and palate is difficult and time-consuming , all previous studies aim ing to differentiate between these two theories have been based on indirect observation of the muscles , rather than direct study of the nerves . METHODS We conducted a prospect i ve study to directly observe and study nerve fibres in uvular specimens from 10 cases of obstructive sleep apnoea , compared with specimens from 10 cases of simple snoring , using transmission electron microscopy .  Five autopsy cases served as controls . RESULTS Obstructive sleep apnoea was associated with definite degenerative changes in myelinated and unmyelinated nerve endings . These degenerative changes were present to a lesser degree and in a smaller proportion of cases of simple snoring . CONCLUSION The events postulated by the neurogenic theory of obstructive sleep apnoea appear to play an important role in the pathophysiology of snoring and obstructive sleep apnoea Sleep-disordered breathing is a common disorder with a range of harmful sequelae . Obesity is a strong causal factor for sleep-disordered breathing , and because of the ongoing obesity epidemic , previous estimates of sleep-disordered breathing prevalence require updating . We estimated the prevalence of sleep-disordered breathing in the United States for the periods of 1988 - 1994 and 2007 - 2010 using data from the Wisconsin Sleep Cohort Study , an ongoing community-based study that was established in 1988 with participants r and omly selected from an employed population of Wisconsin adults . A total of 1,520 participants who were 30 - 70 years of age had baseline polysomnography studies to assess the presence of sleep-disordered breathing . Participants were invited for repeat studies at 4-year intervals . The prevalence of sleep-disordered breathing was modeled as a function of age , sex , and body mass index , and estimates were extrapolated to US body mass index distributions estimated using data from the National Health and Nutrition Examination Survey . The current prevalence estimates of moderate to severe sleep-disordered breathing ( apnea-hypopnea index , measured as events/hour , ≥15 ) are 10 % ( 95 % confidence interval ( CI ) : 7 , 12 ) among 30 - 49-year-old men ; 17 % ( 95 % CI : 15 , 21 ) among 50 - 70-year-old men ; 3 % ( 95 % CI : 2 , 4 ) among 30 - 49-year-old women ; and 9 % ( 95 % CI : 7 , 11 ) among 50 - 70 year-old women . These estimated prevalence rates represent substantial increases over the last 2 decades ( relative increases of between 14 % and 55 % depending on the subgroup ) It has previously been reported that the duration of  obstructive apneas  increases from the beginning to the end of the night ( M. Charbonneau , J. M. Marin , A. Olha , R. J. Kimoff , R. D. Levy , and M. Cosio . Chest 106 : 1695 - 1701 , 1994 ) . The purpose of this study was to test the hypothesis that stimulation of upper airway ( UA ) sensory receptors during obstructed inspiratory efforts contributes to arousal and apnea termination and that a progressive attenuation of this mechanism through the night contributes to apnea lengthening . We studied seven patients ( six men , one woman ) with severe obstructive sleep apnea ( apnea-hypopnea index = 93 + /- 26 events/h ) during two consecutive nights of polysomnographic monitoring .  On one night ( r and om order ) , we performed topical UA anesthesia with 0.2 % tetracaine and on the control night , sham anesthesia . We measured apnea duration , esophageal pressure ( Pes ) during apneas , and apneic O2 desaturation . Consistent with previous findings , apnea duration , number of efforts per apnea , and peak Pes at end apnea increased from the beginning to the end of the control nights . UA anesthesia produced a significant increase in apnea duration at the beginning of the night but no change in apnea length at the end of the night . Peak Pes and the rate of increase in Pes during the anesthesia nights were greater than during control nights , but the rate of increase in Pes was similar for the beginning and end of the control and anesthesia nights . These findings suggest that UA sensory receptors play a role in mediating apnea termination at the beginning of the night but that the contribution of these receptors diminishes as the night progresses such that greater inspiratory efforts are required to trigger arousal , leading to apnea prolongation This study was conducted to determine whether inflammation is present in the uvula mucosa of patients with obstructive sleep apnea ( OSA ) . Uvulas were obtained by uvulopalatopharyngoplasty in 21 patients with moderate OSA ( mean apnea/hypopnea index and st and ard error of the mean : 32 + /- 4 ) and by  autopsy in 5 individuals not known to have OSA . Using point counting in five r and omly selected high-power microscopic fields ( X100 ) , the authors found that the number of leukocytes in the lamina propria of the uvula mucosa was significantly higher in patients with OSA than in the controls ( 179 + /- 12 cells vs. 71 + /- 4 cells , respectively ; P < .05 ) . This was due to a significant increase in the number of plasma cells in patients with OSA as compared with controls ( 89 + /- 15 cells vs. 21 + /- 5 cells , respectively ; P < .05 ) . The thickness of the lamina propria ( an index of interstitial edema ) was also significantly increased in patients with OSA compared with controls ( 0.99 + /- 0.12 mm vs. 0.27 + /- 0.02 mm , respectively ; P < 0.05 ) . The authors conclude that inflammation , characterized by plasma cell infiltration and interstitial edema , is present in the uvula mucosa of patients with moderate OSA . They also suggest that soft palate inflammation contributes to upper airway occlusion observed during sleep in these patients Previous studies support the presence of an upper airway reflex mechanism that contributes to the maintenance of upper airway patency during sleep . We investigated the possibility that interference with this reflex mechanism contributes to the development of  obstructive sleep apnea . Eight otherwise asymptomatic snorers ( seven male and one female ) , age 39 + /- 5.3 yr ( mean + /- SEM ) , underwent overnight sleep studies on three successive nights . An acclimatization night was followed by two study nights r and omly assigned to control ( C ) and oropharyngeal anesthesia ( OPA ) . On the OPA night topical anesthesia was induced using 10 % lidocaine spray and 0.25 % bupivacaine gargle . A saline placebo was used on night C. All subjects slept well on both study nights ( mean sleep duration was 6.2 h on both study nights ) , and sleep stage distribution was similar on both nights . Obstructive apneas and hypopneas ( OAH ) rose from 114 + /- 43 during C to 170 + /- 49 during OPA ( p less than 0.02 ) . Central apneas and hypopneas ( CAH ) were unchanged between the two nights ( 8 + /- 4.9 versus 7 + /- 3 ) . The duration of OAH was similar on both study nights ( 20 + /- 1.9 s during C versus 20 + /- 1.5 s during OPA ) . The frequency of movement arousals terminating OAH tended to be higher during OPA ( 7 + /- 2.9/h ) than during C ( 3 + /- 0.7 ) ; P = NS . The frequency of oxyhemoglobin desaturations was also higher during OPA ( 5 + /- 2.1/h ) than during C ( 3 + /- 1.4 ) , p less than 0.07 . ( ABSTRACT TRUNCATED AT 250 WORDS Previous studies indicate that upper airway ( UA ) sensory receptors play a role in the maintenance of UA patency and contribute to arousal in response to airway occlusion . An impairment of UA sensory function could therefore predispose to UA obstruction during sleep . We hypothesized that UA sensation is impaired in obstructive sleep apnea ( OSA ) , and that sensation improves after treatment with nasal continuous positive airway pressure ( CPAP ) . We measured two-point discrimination ( 2PD ) and vibratory sensation thresholds ( VT ) in 37 patients with OSA ( mean [ + /- SE ] apnea- hypopnea index [ AHI ] = 39 + /- 5 events/h ) , 12 nonapneic snorers ( SN ) , and 15 control subjects ( CL ) . Sensory thresholds were determined in the UA and on the lip and h and as control sites . Both 2PD and VT were similar among the three groups at the lip and h and sites but were significantly reduced in the UA of OSA and SN subjects versus CL ( p < 0.05 ) . Values for 2PD and VT in the UA of OSA versus SN were not significantly different . Sensory measures were repeated after 6 mo in 23 OSA patients treated with CPAP as well as in 18 untreated patients . Thresholds for 2PD and VT at control sites remained identical in both groups , as did 2PD for the UA . However , VT in the UA showed a significant improvement in treated ( 4.4 + /- 0.2 pre-CPAP versus 3.8 + /- 0.2 mm post-CPAP , p < 0.05 ) but not untreated patients . These findings indicate the presence of a selective impairment in the detection of mechanical stimuli in the UA of patients with OSA and SN , which is partially reversible after treatment with nasal CPAP in patients with OSA Snoring is a very common problem but there are few publications on the histological findings of the soft palate/uvula and these lack consistency . The relative proportions of tissue types in the base of the uvula removed from 17 adults who underwent uvulopalatopharyngoplasty for heavy snoring were therefore compared with 14 cadaveric specimens . The mean percentage of muscle from the snoring group was 12.1 % compared with 7.2 % in the control group ( P < 0.05 ) . The percentage of fibrous tissue was greater in the cadavers ( 52.8 % vs 45.5 % in the snorers , P < 0.05 ) . The percentage of muscle was inversely related to the percentage of fibrous tissue in the snoring group ( P < 0.02 ) . We hypothesize that these changes are a consequence of the repetitive forces on the soft palate during snoring rather than being related to the pathogenesis of snoring 
    Output:
    