Objective To observe the eotaxin expression of rat airway smooth muscle cells ( ASMCs) induced by serum from asthmatic rats, and explore the possible mechanism. Methods ASMCs isolated fromrat tracheas were cultured in vivo. Then they were treated with serum from asthmatic rats, or treated with serum and dexamethasone simultaneously. The level of eotaxin protein in supernatant and eotaxin mRNA in ASMCs were measured by ELISA and reverse transcription-polymerase chain reaction. The expression of cAMP in ASMCs was examined by radioimmunoassay. Results After the treatment with sensitized serum, the eotaxin level in supernatant and mRNA expression in ASMCs were significantly higher [ ( 107. 09 ±7. 12) ng/L vs. ( 0. 63 ±0. 56) ng/L, P lt; 0. 05; 1. 39 ±0. 04 vs. 0. 05 ±0. 01, P lt;0. 05] , and the level of cAMP in ASMCs was significantly lower compared with the control group [ ( 17. 58 ±3. 62) ng/L vs. ( 32. 39 ±3. 36) ng/L, P lt; 0. 05] . After intervened by the sensitized serum and dexamethasone simultaneously, the protein and mRNA expressions of eotaxin were lower compared with those intervened by sensitized serumalone [ ( 64. 18 ±4. 04) ng/L and 0. 77 ±0. 19] . The level of eotaxin in supernatant was negatively correlated with cAMP level in ASMCs ( r = - 0. 788, P lt; 0. 01) . Conclusions There is anautocrine function in ASMCs as inflammatory cells after stimulation with sensitized serum. Eotaxin may play an important roll in the pathogenesis of asthma via a cAMP-dependent pathway.
Objective To explore the effects of prolonged inhalation of Aspergillus fumigatus ( Af)spores on epithelial cell injury and expression of epidermal growth factor receptor( EGFR) in airways of asthmatic rats. Methods 64 male Wistar rats were randomly divided into 8 groups, ie. chronic asthma group ( group A) , chronic asthma plus Af spores inhalation for 1 week ( group B) , 3 weeks ( group C) and 5 weeks ( group D) , chronic asthma plus saline inhalation for 5 weeks ( group E) , OVA-sensitized and salinechallenged group ( group F) , and OVA-sensitized and saline-challenged plus Af spores inhalation for 5 weeks ( group G) ( each n =8) . The airway resistance ( Raw) and change of Raw after acetylcholine provocation were detected using a computerized system. The concentrations of epidermal growth factor ( EGF) andtransforming growth factor alpha( TGF-α) in BALF were measured by ELISA. The extents of epithelial cell injury and goblet cell hyperplasia were evaluated on hematoxylin and eosin-stained( HE) and periodic acidschiff ( PAS) stained lung sections. The expression of EGFR in airway epithelia was demonstrated byimmunohistochemistry, and the level of EGFR protein in the rat lung tissues was measured by western blot.Results The concentration of EGF( pg/mL) ( 51. 72 ±8. 54, 68. 12 ±7. 85, 86. 24 ±9. 12, respectively)and TGF-α( pg/mL) ( 55. 26 ±9. 30, 75. 58 ±11. 56, 96. 75 ±14. 66, respectively) , detached/ inner perimeter of epithelium( % ) ( 11. 25 ±3. 12, 26. 45 ±5. 56, 28. 50 ±7. 50, respectively) , the ratio of goblet cell area to epithelial cell area ( % ) ( 16. 42 ±5. 24, 22. 64 ±6. 82, 36. 38 ±9. 21, respectively) , the integrated optical density ( IOD) of EGFR positive stain in airway epithelial cells ( 82 ±15,120 ±19, 165 ±21, respectively) , and the EGFR protein levels in lung tissues ( 0. 91 ±0. 26, 1. 61 ±0. 52, 2. 52 ±0. 78,respectively) in group B, C, and D were higher than those in group A, E, F and G( P lt; 0. 05 or P lt;0. 01) .The change rates of Raw( % ) ( 61. 91 ±5. 26, 84. 69 ±6. 38) in group C and D were higher than those in group A, E, F and G ( P lt; 0. 05 or P lt;0. 01) . The IOD of EGFR was positively correlated with detached/inner perimeter of epithelium( % ) and the ratio of goblet cell area to epithelial cell area( % ) ( r = 0. 692,P lt;0. 01; r = 0. 657, P lt; 0. 01, respectively) . Conclusion Prolonged inhalation of Aspergillus fumigatus spores can aggravate airway epithelial cell injury, up-regulate the expression of EGFR in airway epithelial cell and induce goblet cell hyperplasia, thus increase the airway responsiveness in rats with chronic asthma.
Objective To explore the profile and diagnosis value of airway resistances before and after bronchial dilation test ( BDT) in patients with COPD and asthma. Methods Airway resistances before and after BDT were measured in COPD patients and asthma patients with different severity by impulse oscillometry ( IOS) , and the characteristic changes of the two different diseases were analyzed compared with healthy subjects. Results Airway resistance indexes except X5 were higher in the COPD and the asthma patients than those in the healthy subjects before BDT ( P lt; 0. 05) . There were significant differences in airway resistance indexes except X5 and Rc between the mild asthma patients and the moderate to severe asthma patients. Significant difference in Z5, Fres, and Rp were observed in the mild COPD patientscompared with the moderate to severe COPD patients. There were statistical differences in airway resistance indexes except X5 between the two groups before and after BDT both in the COPD and the asthma patients ( P lt;0. 05) . The rates of change in Z5, Fres, R5, and Rp were higher than those of FEV1% pred, especially higher in the asthma patients than in the COPD patients ( P lt; 0. 05) . Significant negative correlations between FEV1% pred and Z5, Fres, R5, Rp were revealed in the COPD and the asthma patients ( P lt;0. 01) .The correlation between Fres and FEV1% pred was most significant in the COPD and the asthma patients ( r = - 0. 561, - 0. 761) . Conclusion Airway resistances measured by IOS is sensitive indicators in detecting the airflow obstruction in COPD and asthma, and is useful in early and differential diagnosis of COPD and asthma.
Objective To investigate the effect of adiponectin on proliferation of airway smooth muscle cells( ASMCs) , and explore its possible mechanism. Methods ASMCs were derived fromrat airway tissue and were cultured in vitro. RT-PCR was used to verify the expression of adiponectin receptors on ASMCs. Then ASMCs were treated with adiponectin at different concentrations( 5, 10, 20, 40, 80 μg/mL) for different periods of time( 1, 12, 24, 48, 72 hours) , respectively. The absorbsence ratios of adiponectin at different concentrations were determined by MTT assay. The adenosine monophosphate-activated protein kinase( AMPK) and phosphorylated AMPK( pho-AMPK) in ASMCs were quantified by Western blot after being treated with adiponectin at different concentrations ( 5, 10, 20, 40 μg/mL) for 48 hours. ResultsThe inhibition of adiponectin on ASMCs was showed in dose-dependent manner( r = 0. 324, P lt; 0. 01) and time-dependent manner( r = 0. 607, P lt; 0. 05) . Western blot indicated that the expression of pho-AMPK increased with the increased concentrations of adiponectin( r =0. 607, P lt; 0. 01) . The ratio of pho-AMPK/AMPK were ( 27. 66 ±1. 03) % , ( 31. 91 ±0. 86 ) %, ( 75. 52 ±2. 67) % , and ( 84. 50 ±1. 05) % ,respectively, with significant differences between each concentrations of adiponectin( P lt; 0. 05) . There was no expression of pho-AMPK in the control group. Conclusion Adiponectin can significantly inhibit ASMCs’proliferation by activating AMPK.
Obstractive To observe the clinical effects and safety of endobronchial electrocautery treatment for tracheobronchial obstructive lesions in inoperable tracheobronchial squamous cell carcinoma.Methods Ninety-five patients with advanced and inoperable tracheobronchial squamous cell carcinoma were included. Thirty-four patients with central airway obstruction were treated with endobronchial electrocautery plus chemotherapy ( group A) and 61 patients without central airway obstruction were treated with chemotherapy alone ( group B) . The chemotherapy consisted of cisplatin or carboplatin, plus another thirdgeneration chemotherapy agent. Results In groug A, there were mean improvements in FEV1 of 41. 1% and in peak expiratory flow( PEF) of 65. 6% . There was no significant difference in the survival rates of the patients with and without central airway obstruction. Median survival time of group A was 11. 3 months and those of group B was 11. 6 months. 3, 6, and 12-month survival rates in group A were 87% , 68% and 39% respectively, and those in group B were 93% , 76% , and 45% respectively. Conclusion Endobronchial electrocautery is an effective and safe approach for inoperable tracheobronchial obstructive malignancies with few complications.
Objective To invesitgate the relationship between 8-isoprostane ( 8-iso-PG) level in exhaled breath condensates ( EBCs) and severity of asthma and explore the role of 8-iso-PG in asthma evaluation and monitoring. Methods Fifty-nine patients with asthma were enrolled. In which 15 cases were acute exacerbation, 13 cases were mild intermittent, 15 cases were mild persistent, and 16 cases were moderate-to-severe persistent. Thirteen healthy volunteers were recruited as control. EBCs were collected using EcoScreen system. The 8-iso-PG levels in EBCs were measured by a specific enzyme immunoassay.The patients with mild intermittent asthma were treated with inhaled corticosteroid ( ICS) for one month and their EBCs were recollected for 8-iso-PG measurement. Results Exhaled 8-iso-PG levels were obviously increased in the patients with acute asthma compared with those chronic asthmatics [ ( 47. 2 ±6. 8) pg/mL vs ( 24. 5 ±12. 0) pg/mL, P lt; 0. 01] . In the chronic persistent asthma, the levels were significantly higher in patients with mild persistent and moderate-to-severe asthma [ ( 17. 9 ±1. 2) pg/mL and ( 39. 7 ±4. 0) pg/mL,P lt; 0. 01] . While 8-iso-PG level did not differ significantly in intermittent asthma [ ( 13. 5 ±1. 1) pg/mL]compared with the control subjects ( P gt; 0. 05 ) . After one-month ICS treatment the 8-iso-PG level in the patients with mild intermittent asthma did not change significantly although the ACT score improved. Conclusions 8-iso-PG levels in EBC are associated with the severity of asthma, implicating 8-iso-PG may be useful in monitoring airway oxidative stress in asthma. ICS treatment is incapable of decreasing the 8-iso-PG, suggesting the ICS has minor impact on oxidative stress.
Objective To explore the relationship between obstructive sleep apnea hypopnea syndrome ( OSAHS) and airway hyperresponsiveness ( AHR) . Methods 197 subjects suspected for OSAHS were enrolled in the study. They were all performed overnight polysomnogram ( PSG) monitoring and lung function test. Acoording to the results of FEV1% pred, they were performed bronchial provocation test( BPT)or brochial dilation test( BDT) . The relation between apnea hypopnea index ( AHI) and the degree of airway hyperresponsiveness ( AHR, expressed as PD20 -FEV1 ) was evaluated by linear correlation analysis. Results 117 patients were diagnosed as OSAHS, in which 28 cases were complicated with AHR( 3 cases with positive BDT result, 25 cases with AHR) . In 80 non-OSAHS patients, 7 cases were complicated with AHR. Theincidence of AHR was higher in the OSAHS patients compared with the non-OSAHS patients( 23. 9% vs 8. 8% , P lt; 0. 01 ) . AHI of OSAHS patients with AHR was higher than OSAHS patients without AHR[ ( 30. 3 ±5. 1) /h vs ( 23. 7 ±2. 4) /h, P lt;0. 01] . There was a positive correlation between AHI and degree of AHR in OSAHS patients with AHR( r=0. 62, P lt;0. 05, n=25) . Conclusion OSAHS is associated with an increased risk of AHR.
Objective To investigate the application and long-termresults of epiglottic in reconstruction of the traumatic laryngotracheal stenosis.Methods From January 1988 to February 2002, 42 patients with traumatic laryngotracheal stenosis were treated, including 33 laryngeal stenosis and9 laryngotracheal stenosis. The following surgical treatment were performed: ① lowered epiglottic andbi-pedicled sternohyoid myofascial flap and ② lowered epiglottic and bipedicledsternohyoid myofascial flap and sternocleidomastoideus clavicle membrane flap. Results Thirty-seven patients(88.1%) were successfully decannulated 10 to 75 daysafter operation. Feeding tube lasted from 9 to 24 days, all the patients rehabilitated deglutition after surgery. The time of using stent was 9 to 19 days in 25cases.All patients were followed up 1 year to 3 years and 4 months. The function of larynx recovered completely in 37 decannulated patients and partially in 5cannulated patients. Conclusion Epiglottic- has the advantages of easy gain, high antiinfection and survival rate, and stable structure. A combination of epiglottic and the bipedicled sternohyoid myofascial flap plus sternocleidomastoideus clavicle membrane flap can repair large laryngeal and tracheal defects.
Respiratory oscillometry is a lung function test that measures the mechanical properties of respiratory system by the forced oscillation technique. Oscillometry can be used in those who cannot perform traditional lung function tests, including young children. It is also an important tool to assess small airways function in clinical and research fields. In 2020, the European Respiratory Society published a new technical standard for respiratory oscillometry, which offered updated technical recommendations on the hardware, software, testing protocols and quality control of oscillometry measurements. This paper interpreted the new technical standard, for providing technical suggestions regarding oscillometry measurements in clinical and research settings, and as a reference for developing technical statements and recommendations for oscillometry in China.
Objective To investigate the effects of smoking intensity, duration and cessation on mRNA and protein expressions of matrix metalloproteinase-9 ( MMP-9) in tracheal epitheliumof rats, and the relationship between smoking or smoking cessation and airway remodeling in chronic obstructive pulmonary disease ( COPD) . Methods Forty Wistar rats were randomly divided into 5 groups, ie. a normal control group, a long termheavy smoking group, a short termheavy smoking group, a long termlight smoking group,and a smoking cessation group which was exposed to room air for 10 weeks after long term heavy smoking.The expressions of MMP-9 mRNA and protein in tracheal epithelium of rats were detected by in situ hybridization and munohistochemistry respectively. Results ( 1) The pathological changes of emphysema were observed in the lung tissue of every smoking rat, and were most sever in the long term heavy smoking group. ( 2) Compared with the normal control group [ ( 0. 88 ±0. 88) PU, ( 2. 80 ±1. 66) PU] , the expressions of MMP-9 mRNA and proteins in tracheal epithelium were remarkable elevated in the long term heavy smoking group [ ( 22. 01 ±2. 86) PU, ( 20. 81 ±2. 46) PU] , the short term heavy smoking group [ ( 14. 94 ±3. 46) PU, ( 13. 68 ±2. 00) PU] , the long term light smoking group [ ( 6. 92 ±2. 71) PU,( 8. 84 ±1. 80) PU] and the smoking cessation group [ ( 19. 00 ±3. 36) PU, ( 14. 82 ±1. 74) PU] ( P lt;0. 01) . Compared with the long term heavy smoking group, the expressions of MMP-9 in tracheal epithelium were decreased in other three smoking groups ( P lt; 0. 05) . Conclusions Smoking could increase the expression of MMP-9 in tracheal epithelium and cause trachea damage and remodeling with intensity and duration in rats. Smoking cessation could decrease the MMP-9 expression and alleviate trachea remodeling,suggesting its role in the prevention of COPD.