ABSTRACT
Objective To investigate the clinical features of patients with bronchiectasis of different types.Methods One hundred and twenty two patients with bronchiectasis at stable stage were recruited from January 2014 to July 2015.The patients were typed as cystic bronchiectasis (n =45) or non-cystic bronchiectasis (n =77) by high resolution CT (HRCT),expectoration bronchiectasis (n =80) or dry brochiectasis (n =42) by clinical symptoms,bacterial colonization (n =42) or non-bacterial colonization (n =80) by sputum culture.The modified British Medical Research Council (mMRC) dyspnea scale,Leicester Cough Questionnaire (LCQ),St George's Respiratory Questionnaire (SGRQ) and pulmonary function test were used to assess the clinical features,and the episodes of exacerbations and hospitalization,and mortality during 1-year follow-up were documented.Results mMRC dyspnea scale (1.90 ± 0.94 vs.2.90±1.09,t=-5.040),LCQ (16.20±4.60 vs.11.20±2.20,t=8.114),SGRQ (36.80±13.10 vs.52.06±22.10,t=-4.780),FEV1％ pred (68.45 ±26.50 vs.52.22 ±20.60,t=3.458),FVC％ pred (72.20 ±26.32 vs.63.10 ±21.42,t =2.058),FEV1/FVC (75.14 ±20.52 vs.58.12 ± 19.82,t =4.546),diffusing capacity of the lung for carbon monoxide (DLCO) (76.24 ± 28.40 vs.54.32 ± 21.20,t =4.400),episodes of exacerbations (Z =-8.272) and hospitalization during 1-year follow-up [6(14.29％) vs.29(36.25％),x2 =6.495] in patients with dry bronchiectasis were significantly better than those in patients with expectoration bronchiectasis (all P ＜ 0.05).mMRC dyspnea scale (3.20 ± 2.10vs.2.10±1.40,t=3.131),LCQ (10.12±2.63vs.16.22 ±3.22,t=11.365),SGRQ (54.80± 18.12 vs.34.06 ± 12.10,t =6.839) and FEV1％ pred (46.52 ± 22.55 vs.58.22 ± 24.62,t=-2.611),FVC％ pred (60.24± 18.22 vs.70.10±24.20,t =-2.547),FEV1/FVC (62.54± 19.02vs.73.12 ±18.42,t=-3.025),DLCO (62.24 ±22.40 vs.74.52 ±26.26,t=-2.627),episodes of exacerbations (Z =10.213) and hospitalizations during 1-year follow-up [21 (46.67 ％) vs.14 (18.18％),x2 =1 1.260] in patients with cystic bronchiectasis were significantly more severe than those in patients with non-cystic bronchiectasis (all P ＜ 0.05).mMRC dyspnea scale (2.38 ± 1.45 vs.1.92 ± 1.14,t =2.175),LCQ (12.82 ±2.12 vs.16.20 ±3.96,t =-6.140),SGRQ (54.22±21.50 vs.41.20 ± 14.60,t =3.521) and FEV1 ％ pred (54.20 ± 21.60 vs.66.45 ± 28.24,t =-2.668),FVC％ pred (63.10 ±24.32 vs.73.46 ±25.30,t =-2.177),FEV1/FVC (62.22 ±20.80 vs.72.14 ±24.36,t =-2.243),DLCO (58.52 ± 20.42 vs.69.22 ± 25.60,t =-2.344),episodes of exacerbation (Z =19.352) and hospitalization during 1-year follow-up [19 (45.24％) vs.16 (20.00％),x2 =8.575] in patients with bacterial colonization bronchiectasis were significantly more severe than those in patients with non-bacterial colonization bronchiectasis (all P ＜ 0.05).However,there was no significant difference in mortality during 1-year follow-up (all P ＞ 0.05) among patients with different types of bronchiectasis.Conclusion Patients with cystic,bacterial colonization and expectoration types of bronchiectasis seem to have more severe symptoms,more episodes of exacerbations and hospitalizations than those of non-cystic,non-bacteria colonization and dry types of bronchiectasis.
ABSTRACT
Objective To explore the effect of low-dose cyclophosphamide(CTX)on apoptosis of implanted human lung carcinoma in nude mice.Methods BALB/c nude mice bearing lung carcinoma were randomized into several groups,each receiving different dose of CTX respectively.We investigated antitumor effect and toxicity of CTX.At the end of experiment,tumors were resected for immunohistochemical staining.Nuclear factor ?B(NF-?B P65)was detected and apoptosis was measured by TUNEL.Morphological changes of tumor cells were observed.Results The volume of tumors was much smaller in mice receiving continuous low-dose CTX than that receiving maximally tolerated dose of CTX and normal saline(control group).The apoptotic index was increased and NF-?B P65 decreased in the mice receiving low-dose of CTX.Conclusion The continuous low-dose of CTX inhibits the growth of implanted tumor and increases tumor cell apoptosis,which may be due to the down-regulation of nuclear factor ?B.