目的报告32例膈肌破裂与创伤性膈疝的诊治体会。方法对该院收治的32例创伤性膈肌破裂进行回顾性分析。结果该32例中，开放性损伤12例，闭合性损伤20例，26例并发创伤性膈疝。经X线检查，18例有阳性发现； 16例行CT检查，结果均为阳性； 术前确诊24例（75%），治愈28例，死亡4例（12.5%）。结论CT和X线检查是诊断膈肌破裂和创伤性膈疝的主要依据。早期诊断、及时手术治疗是提高治愈率、降低死亡率的关键。
Objective To investigate the protective effects of recombinant human insulin-like growth factor-1 ( rhIGF-1) on apoptosis of diaphragm in rats with COPD and its impact on pulmonary function. Methods Forty-five male Wistar rats were randomly divided into three groups, ie. a normal control group, a model group, and an IGF-1 intervention group, with 15 rats in each group. The rats in the model group and IGF-1 group were exposed to 5% smoke ( 30 min perday, lasting 28 days) in a sealed box, and 200 μg lipopolysaccharide was injected intratracheally on the 1st and 14th day. The rats in the IGF-1 group were given rhIGF-1 ( 60 μg /100 g) additionally by subcutaneous injection once a day, lasting 28 days. On the 1st, 14th, 28th day, 5 rats from each group were sacrificed. The weight, rate of apoptosis, Fas gene and Fas protein expression of isolated diaphragms were detected. The pulmonary function was measured on the 28th day before sacrificed. Results The mass of diaphragms, minute ventilation ( VE) , peak expiratory flow ( PEF) , inspiratory capacity ( IC) , forced expiratory volume in 0. 3 second ( FEV0. 3) of themodel groupand IGF-1 group were all decreased compared with the control group ( P lt; 0. 05) . The mass of diaphragms, VE, IC of the IGF-1 group were higher than those of the model group ( P lt;0. 05) , and the differences of PEF and FEV0. 3 were not significant ( P gt; 0. 05) . On the 14th, 28th day, rate of apoptosis, Fas gene and protein expressions in the IGF-1 group were lower than those in the model group, and still higher than those in the control group ( P lt; 0. 05) . Conclusions Fas/FasL mediated apoptosis way is involved in the diaphragm apoptosis. rhIGF-1 may reduce the apoptosis of the diaphragmand improve the VE and IC of rats with COPD by intervening Fas/FasL pathway.
Objective To study the role of ubiquitin-proteasome pathway in diaphragm of COPD rats. Mathods Thirty rats were divided into a normal control group and a COPD group. COPD model was established by exposure to cigarette smoke for three months. The protein levels of E2-14k and proteasome subunit C8 in diaphragms were measured by Western blot. The mRNA levels of ubiquitin and proteasome subunit C2 in diaphragms were measured bymeans of realtime polymerase chain reaction( RT-PCR) . Results Compared with the control group, the protein expression of E2-14k increased significantly in the COPD group ( 0. 81 ±0. 28 vs 0. 50 ±0. 25, P lt;0. 05) , but C8 protein level was not significantly different between the two groups( P gt;0. 05) . The mRNA expression of ubiquitin increased significantly in the COPD group( 0. 89 ±0. 20 vs 0. 50 ±0. 15, P lt;0. 05) , but C2 mRNA level was not significantly different between the two groups ( P gt; 0. 05 ) . Conclusions The mRNA and protein expressions of ubiquitin-proteasome pathway in diaphragmincreased significantly in COPD rats, suggesting that the activity of ubiquitin-proteasome pathwayincreased, which lead to an increase of protein degradation.
Objective To investigate the expressions of ubiquitin-proteasome markers，including E2-14K，MAFbx，MuRF-1，and nuclear factor-κB（NF- κB） p50，in diaphragm of COPD rats，and their relationship with IL-17 level in diaphragm and serum in order to elucidate the potential mechanism of diaphragm atrophy. Methods Thirty healthy adult male SD rats were randomly divided into a model group （n=18） and a normal control group （n=12）. The COPD rat model was established by instillation of lipopolysaccharide （LPS） and exposure to cigarette smoke for 28 days. The protein levels of E2-14K，MAFbx，MuRF-1，and NF-κB p50 in diaphragm were measured by Western blot. The concentration of IL-17 in serum and diaphragm was measured by ELISA. Results Western blot showed that the protein expressions of E2-14K，MAFbx，MuRF-1，and NF-κB p50 in diaphragm increased significantly in the COPD model group compared with the normal control group （0.96±0.12 vs. 0.53±0.09，0.99±0.10 vs. 0.53±0.08，0.95±0.08 vs. 0.51±0.16，1.11±0.10 vs. 0.64±0.50，respectively，Plt;0.01）. The IL-17 level in serum and diaphragm was significantly higher in the COPD group than the control group. The expression of NF-κB p50 was positively correlated with E2-14K，MAFbx，and MuRF-1 expressions （r=0.82，0.92，0.86，respectively，Plt;0.01）. Both in serum and diaphragm，IL-17 level was positively correlated with the percentage of neutrophils，levels of NF-κB p50，E2-14K，MAFbx，and MuRF-1 expressions（all Plt;0.01）. The IL-17 levels in serum and diaphragm were also positively correlated each other （r=0.84，Plt;0.01）. Conclusions The results show that the ubiquitin-proteasom pathway，the NF-κB pathway and IL-17 are up-regulated in diaphragm of COPD rats .These alterations may contribute to diaphragm atrophy in COPD.