To investigate cyclooxygenase-2 (COX-2) mRNA expression in human esophageal squamous cell carcinoma and the effect of a non-steroidal anti-inflammatory drug (NSAID) on it, in order to explore the mechanism of COX-2 in esophageal squamous cell carcinoma (ESCC) carcinogenesis and the ability of NSAID to prevent or treat ESCC. Frozen specimens of human ESCC and adjacent normal esophageal squamous epithelium pairs (n = 22) were examined for COX-2 mRNA expression by reverse-transcription polymerase chain reaction (RT-PCR). After incubation with aspirin (a non-selective COX inhibitor) or Nimesulide (a selective COX-2 inhibitor), the proliferation status of two human esophageal squamous cancer cell lines, EC-9706 and EC-109, was quantified by 3-(4,5-dimethyl-thiazol-2yl)-2,5-diphenyltetrazolium bromide assay. The expression of COX-2 mRNA in these cells was detected by RT-PCR. COX-2 mRNA was expressed in 12 of 22 (54.5%) ESCC tissue samples, but it was undetectable in all the specimens of adjacent normal esophageal squamous epithelium COX-2 mRNA expression. Both aspirin (5-20 mmol/L) and Nimesulide (0.1-0.8 mmol/L) inhibited EC-9706 cell line proliferation and suppressed its COX-2 mRNA expression dose-dependently. However, only aspirin (5-20 mmol/L) could inhibit proliferation in the EC-109 cell line and suppress COX-2 mRNA expression. Nimesulide (0.1-0.8 mmol/L) could neither inhibit EC-109 cell growth nor suppress COX-2 mRNA expression. COX-2 mRNA expression is a frequent phenomenon in human ESCC tissue samples and plays an important role in the carcinogenesis of ESCC. NSAID may be useful in the chemoprevention and therapy of human ESCC and its effects are likely to be mediated by modulating COX-2 activity.

Background and purpose In‐hospital complications after stroke represent barriers to optimal recovery and are even potentially life‐threatening. Anemia is common in stroke patients and is related to poor outcome after stroke. Less is known, however, of the association of anemia with complications. We aimed to investigate the impact of anemia on a series of in‐hospital complications after ischemic stroke. Methods Consecutive patients with ischemic stroke within 7 days were included. Anemia on admission and its severity were defined according to World Health Organization criteria. Eight pre‐specified complications, such as pneumonia, gastrointestinal bleeding (GIB) and hemorrhagic transformation, were recorded during hospitalization. Results A total of 2647 patients were included. Anemia was present in 648 patients (24.5%), and 883 patients (33.4%) experienced at least one complication. Patients with anemia were more likely to experience one or more complications, pneumonia, GIB and thromboembolism (all P < 0.001) than patients without anemia. After adjustment for the confounders, patients with anemia had an adjusted odds ratio for at least one complication of 1.539 [95% confidence interval (CI), 1.232–1.923], for pneumonia of 1.707 (95% CI, 1.345–2.167), for GIB of 2.245 (95% CI, 1.215–4.148) and for thromboembolism of 3.443 (95% CI, 1.668–7.108). The risk of at least one complication, pneumonia, GIB and thromboembolism increased with anemia severity (all P < 0.05). There was no significant association between anemia and urinary tract infection, hemorrhagic transformation, seizures and brain herniation. Conclusion Anemia is an independent predictor of in‐hospital complications following stroke, especially for pneumonia, GIB and thromboembolism. It remains to be studied whether prophylaxis and treatment of anemia would prevent in‐hospital complications.