AIM: To confirm that the inflammation response after mechanical arterial injury correlates with the neointimal hyperplasia in animal model. METHODS: Male Wistar rats underwent left common carotid balloon angioplasty were injected twice with a bacterial lipopolysaccharide (LPS, 50 ng/rat) before and after surgery. Next, just after neointima formation, the animals were sacrificed for the evaluation by morphometric analysis, histological observation and immunostaining. Western blot was used to investigate the protein expression of several known mediators of apoptosis. RESULTS: Serum interleukin-1 beta levels as a marker of inflammation were increased after LPS treated. Early neotimal lesions were characterized by intimal thickening and the presence of SMCs. Neointima with smooth muscle alpha-actin negative were observed at 7 days after injured. These areas of neointima demonstrated a relatively high proliferation index by proliferating cell nuclear antigen (PCNA) antibody staining, whereas the proliferation index in media was low. Neointimal thickness was significantly increased at 4 weeks after injury in LPS treated animals compared with controls, from (151.2?14.5 to 173.9?15.3) ?m2. Activation of caspase-3 was observed, indicating that smooth muscle cells of neointima was associated with apoptosis. Immunofluorescence analysis revealed NF-?B expression located to the adventitia. CONCLUSIONS: Our results indicate that nonspecific stimulation of low-level LPS facilitates neointimal formation and may be an important factor in the restenosis of angioplasty.

BACKGROUND:The elderly hip fracture patients with chronic obstructive pulmonary disease (COPD) have a higher postoperative mortality than those only with hip fractures. In recent years, it has become an issue of concerns. Because the mechanism is unknown, however, there are no effective clinical interventions for these patients. OBJECTIVE:To observe the effect of bone marrow stromal stem cel s (BMSCs) on the level of pulmonary inflammation in aged rats with chronic obstructive pulmonary disease (COPD) after hip fractures. METHODS:Thirty male Sprague-Dawley rats, 12 months old, were exposed to smoking for 4 months and randomized into three groups, smoking, smoking+hip fracture+normal saline, smoking+hip fracture+BMSCs groups. Animal models of hip fracture were made in the latter two groups. Twenty-four hours after hip fracture, the lower lobe and peripheral blood samples were taken from al rats in the three groups, to evaluate the pathological changes of lung tissue and detect levels of inflammatory factors in the lung tissue and peripheral blood. RESULTS AND CONCLUSION:After closed hip fracture, aged COPD rats exhibited inflammatory cel infiltration, mucus secretion, airway stenosis or occlusion;the levels of interleukin-6, tumor necrosis factor-αand interleukin-10 in the lung tissue and peripheral blood were increased. After intravenous injection of BMSCs, the pathological changes of the lung tissue were reduced, and the levels of pro-inflammatory factors, tumor necrosis factor-αand interleukin-6, decreased, but the level of anti-inflammatory factor interleukin-10 further increased, which were significantly different from those in the normal saline group (P<0.05). These findings indicate that BMSCs can relieve acute lung injury in aged COPD rats with hip fractures.

Objective:To evaluate the effect of imatinib on growth impairment in children with chronic myeloid leukemia (CML-CP) in the chronic phase.Methods:From July 2018 to July 2019, questionnaires were distributed to CML children aged <18 years at the time of diagnosis who were receiving imatinib for at least 3 months or to their parents in China. The height-for-age standard deviation score (HtSDS) and the difference of standard deviation integral (△HtSDS) were used to explore the change in height with imatinib therapy.Results:The data of 238 respondents were included; 138 (58.0% ) respondents were men. The median age at the first diagnosis of CML was 11.0 years (range, 1.4-17.9 years) , and 93 (39.0% ) respondents were at the prepuberty stage. At the time of completing the questionnaires, the median age was 15.0 years (range, 2.0-34.0 years) . The median duration of imatinib therapy was 28 months (range, 3-213 months) . Among all the respondents, the mean HtSDS when completing the questionnaires (-0.063±1.361) was significantly lower than that at the time of starting imatinib treatment (0.391±1.244) ( P<0.001) . Total 71.0% respondents showed growth impairment that was more common in those starting imatinib therapy at prepubertal age than in those starting at pubertal age. Multivariate analysis showed that younger at the start of imatinib therapy ( P<0.001) and longer duration of imatinib therapy ( P<0.001) were significantly associated with severe growth impairment on imatinib therapy. Conclusions:Imatinib induced growth impairment in children with CML-CP. Younger the age of initiation and longer the duration of imatinib therapy, more obvious the effect of imatinib on growth impairment.