目的分析学龄前儿童腺样体肥大合并分泌性中耳炎(Otitis media with effusion, OME)的发病危险因素。方法选取住院腺样体肥大患儿,以是否合并OME分组,比较一般临床资料、血清过敏原筛查结果、鼻咽部分泌物及腺样体组织的菌群分布情况。...目的分析学龄前儿童腺样体肥大合并分泌性中耳炎(Otitis media with effusion, OME)的发病危险因素。方法选取住院腺样体肥大患儿,以是否合并OME分组,比较一般临床资料、血清过敏原筛查结果、鼻咽部分泌物及腺样体组织的菌群分布情况。结果 OME组患儿年龄中位数低于对照组,OME发生率随年龄增长逐渐下降;OME组曾有急性中耳炎病史的患儿高于对照组;OME组食入性过敏原阳性项数高于对照组,其中牛奶、鸡蛋白差异更显著;OME组腺样体组织条件致病菌检出率高于对照组,其中流感嗜血杆菌检出率差异更显著。以上差异均有统计学意义。结论对于学龄前腺样体肥大合并分泌性中耳炎患儿,低龄是其发病的主要因素,急性中耳炎史、食入性过敏原刺激、腺样体组织条件致病菌存在可能是其发病的不良因素。展开更多
OBJECTIVE: To study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro. METHODS: PIM were isolated and cultured in the presence o...OBJECTIVE: To study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro. METHODS: PIM were isolated and cultured in the presence or absence of LPS, CCK-8, proglumide (the antagonist of CCK receptors) and vehicle. The expression of membrane CD14 (mCD14) protein was assayed by flow cytometry and soluble CD14 (sCD14) in the supernatant was analyzed semi-quantitatively by Western blot. TNF-alpha in the supernatant was detected with ELISA. RESULTS: CCK-8, at concentrations of 10(-7) mol/L and 10(-6) mol/L, significantly inhibited the expression of mCD14. Release of sCD14 and TNF-alpha in the supernatant was up-regulated by LPS (1 microg/ml) but reduced by CCK-8. The effect of CCK-8 was inhibited by proglumide. CONCLUSION: CCK-8 negatively modulated several functions of LPS-stimulated PIM through CCK receptors. This may be one of the mechanisms for CCK-8 to alleviate inflammation in lung tissue during endotoxemia.展开更多
文摘目的分析学龄前儿童腺样体肥大合并分泌性中耳炎(Otitis media with effusion, OME)的发病危险因素。方法选取住院腺样体肥大患儿,以是否合并OME分组,比较一般临床资料、血清过敏原筛查结果、鼻咽部分泌物及腺样体组织的菌群分布情况。结果 OME组患儿年龄中位数低于对照组,OME发生率随年龄增长逐渐下降;OME组曾有急性中耳炎病史的患儿高于对照组;OME组食入性过敏原阳性项数高于对照组,其中牛奶、鸡蛋白差异更显著;OME组腺样体组织条件致病菌检出率高于对照组,其中流感嗜血杆菌检出率差异更显著。以上差异均有统计学意义。结论对于学龄前腺样体肥大合并分泌性中耳炎患儿,低龄是其发病的主要因素,急性中耳炎史、食入性过敏原刺激、腺样体组织条件致病菌存在可能是其发病的不良因素。
文摘OBJECTIVE: To study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro. METHODS: PIM were isolated and cultured in the presence or absence of LPS, CCK-8, proglumide (the antagonist of CCK receptors) and vehicle. The expression of membrane CD14 (mCD14) protein was assayed by flow cytometry and soluble CD14 (sCD14) in the supernatant was analyzed semi-quantitatively by Western blot. TNF-alpha in the supernatant was detected with ELISA. RESULTS: CCK-8, at concentrations of 10(-7) mol/L and 10(-6) mol/L, significantly inhibited the expression of mCD14. Release of sCD14 and TNF-alpha in the supernatant was up-regulated by LPS (1 microg/ml) but reduced by CCK-8. The effect of CCK-8 was inhibited by proglumide. CONCLUSION: CCK-8 negatively modulated several functions of LPS-stimulated PIM through CCK receptors. This may be one of the mechanisms for CCK-8 to alleviate inflammation in lung tissue during endotoxemia.
