Diagnosis and treatment of late spontaneous esophageal rupture:a report of 10 cases / 中国基层医药

Objective To summarize and analyze the clinical features,diagnostic methods and treatment measures of patients with advanced spontaneous esophageal rupture. Methods Retrospective analysis of clinical characteristics of 10 patients with advanced spontaneous esophageal rupture was conducted. Results The average age of the patients was 49. 3 years old. The average time of diagnosis was 82. 6 hours. The cause of onset was drastic vomiting except for one case falling down. The main clinical manifestations were chest pain,abdominal pain,and shortness of breath,fever and elevation of hemogram,pleural effusion appeared in all patients,1 case was not treated in time,and 9 cases of the first checks were delayed for diagnosis and treatment in other specialties. Conservative treatment(closed thoracic drainage,gastrointestinal decompression,enteral nutrition support and antimicrobial therapy) was given to all patients. All 10 cases were cured by conservative treatment,the average time of hospitalization was 49. 4 days,followed up for 2 years, no chronic empyema, stricture of the esophagus and reflux esophagitis were observed. Conclusion Late spontaneous rupture of the esophagus is caused by delays in the diagnosis and treatment of the esophagus,the effect of comprehensive conservative treatment is satisfactory.

Chlorogenic-induced inhibition of non-small cancer cells occurs through regulation of histone deacetylase 6.

Chlorogenic acid (CGA), an ester with various pharmacological effects, is important in cancer therapy. However, the specific antitumor mechanism of CGA is not entirely clear, especially with respect to its suppression of non-small cell lung cancer (NSCLC). The present study was carried out to assess the effect of CGA on NSCLC, and the mechanism involved. Cell viability assay and colony formation assay revealed that CGA blocked the proliferative capacity of NSCLC cells in vitro. Results from the migration assay suggested that CGA also inhibited the migration of A549 cells. Other assays further revealed that CGA strongly and selectively inhibited histone deacetylase 6 (HDAC6) activity and suppressed the activity of matrix metalloproteinase-2 (MMP-2) through decreased expression of Ac-NF-κB. Tumorigenicity assay showed that CGA also inhibited the proliferation and metabolism of NSCLC in vivo. These results indicate that CGA significantly suppresses the proliferation of NSCLC by regulating the activity of histone deacetylase 6.