Xie F.,Tianjin First Central Hospital
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology | Year: 2011
This study was to establish an iron overload bone marrow (BM) model by co-culturing the mononuclear cells from BM with iron, and investigate its hematopoiesis changes. The iron overload model was set up by adding different concentration of ferric citrate (FAC) into the mononuclear cells from BM and culturing for different time, and the model was confirmed by detecting labile iron pool (LIP). Then the apoptosis of hematopoietic cells, ability of hematopoietic colony forming (CFU-E, BFU-E, CFU-GM and CFU-mix) and percentage of the CD34(+) cells of the BM cells all were determined. The changes of these indexes were tested after the iron-overloaded BM was treated with deferasirox (DFO). The results showed that after BM cells were cultured with FAC at different concentrations for different time, the LIP increased in time-and concentration-dependent manners. The intracellular LIP reached maximum level when cultured at 400 μmol/L of FAC for 24 hours. The detection of BM cell hematopoietic function found that the apoptotic rate of the FAC-treated cells (24.8 ± 2.99%) increased significantly, as compared with normal control (8.9 ± 0.96%)(p < 0.01). The ability of hematopoietic colony forming in FAC-treated cells decreased markedly, as compared with normal control (p < 0.05). The percentage of CD34(+) cells of FAC-treated cells (0.39 ± 0.07%) also decreased significantly, as compared with normal control (0.91 ± 0.12%)(p < 0.01). And these changes could be alleviated by adding DFO. It is concluded that the iron-overloaded model has been set by adding iron into the mononuclear cells from BM in vitro, and the hematopoietic function of iron-overloaded BM is deficient. These changes can be alleviated by removing the excess iron from the BM cells through treating with DFO. These findings would be helpful to further study the mechanism of iron-overload on the hematopoiesis of BM and also useful to find the way to treat iron-overload patients with hematopoietic disorders.
Wang W.L.,Tianjin First Central Hospital
The American journal of emergency medicine | Year: 2015
Pulmonary toxicity has frequently been recognized as a potentially serious complication associated with sirolimus therapy. It consists of a wide spectrum of syndromes most characterized by the presence of lymphocytic alveolitis and lymphocytic interstitial pneumonitis. The most commonly presenting symptoms are fever and dyspnea. Chest computed tomography generally reveals bilateral, patchy, or diffuse alveolointerstitial infiltrates. The discontinuation or dose reduction of sirolimus usually leads in most cases to a good outcome with complete clinical and radiologic resolution. However, to establish a diagnosis is difficult because of the absence of specific diagnostic criteria, and in rare cases, it could be fatal or life threatening when the diagnosis was delayed. Here, we reported 2 severe cases of acute respiratory distress attributed to the therapy of sirolimus in solid organ transplant recipients. Although the diagnostic course was difficult, withdrawal of sirolimus and temporary administration of steroids eventually resulted in a rapid recovery in both 2 patients. In addition, possible mechanisms, clinical characteristics, approach to diagnosis, and treatment strategies of sirolimus-induced pulmonary toxicity were also discussed in this article.
Zhang W.X.,Tianjin First Central Hospital
Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases | Year: 2012
To investigate the effect of prostaglandins E1 combined with Xuebijing injection on the expression of transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α (TNF-α) in rats with acute pulmonary interstitial fibrosis. A rat model of pulmonary interstitial fibrosis was established by intratracheal injection of bleomycin (1 ml/kg). One hundred and eight Wistar rats were randomly divided into six groups with 18 in each group, which were normal control group, model group, hormone (methylprednisolone) treatment group, Xuebijing treatment group, prostaglandin E1 treatment group and combination treatment group (prostaglandin E1 and Xuebijing injection). Except for those in the normal control group, the rats in each group were sacrificed on the 7th, 14th and 28th day after treatment. The TGF-β1 expression in lung tissue was measured by immunohistochemical staining. The TNF-α concentration in bronchoalveolar lavage fluid (BALF) of rat model was determined by enzyme-linked immunosorbent assay. The combination treatment group showed significantly more macrophages with TGF-β1 expression in lung tissue at each time point, as compared with the model group, Xuebijing treatment group, methylprednisolone treatment group and prostaglandin E1 treatment group (P < 0.05). On the 7th day, the TNF-α concentration in BALF in the combination treatment group was significantly lower than those in the model group, methylprednisolone treatment group and prostaglandin E1 treatment group (P < 0.05); on the 14th day, the TNF-α concentration in BALF in the combination treatment group was significantly lower than that in the model group (P < 0.05); on the 28th day, the levels of TNF-α in the prostaglandin E1 treatment group and combination treatment group were significantly lower than that in the model group (P < 0.05). Prostaglandin E1 combined with Xuebijing injection may significantly inhibit TGF-β1 expression in the lung tissue of rats with acute pulmonary interstitial fibrosis, which reduces alveolar inflammatory response.
Li Y.,Harvard University |
Wang W.,Tianjin First Central Hospital |
Wang W.,Harvard University |
Winkelman J.W.,Harvard University |
And 3 more authors.
Neurology | Year: 2013
Objective: To prospectively examine whether men with restless legs syndrome (RLS) had an increased risk of mortality. Method: This was a prospective cohort study of 18,425 US men free of diabetes, arthritis, and renal failure in the Health Professionals Follow-up Study (HPFS). In 2002, RLS was assessed using a set of standardized questions. Deaths were identified from state vital statistics records, the National Death Index, family reports, and the postal system. Results: During 8 years of follow-up (2002-2010), we documented 2,765 deaths. In an age-Adjusted model, RLS was associated with a 39% increased risk of mortality (hazard ratio [HR] 5 1.39; 95% confidence interval [CI] 1.19-1.62; p , 0.0001). The association between RLS and mortality was slightly attenuated after further adjustment for body mass index, lifestyle factors, chronic conditions, sleep duration, and other sleep-related disorders (adjusted HR5 1.30; 95%CI 1.11-1.52; p5 0.003). When we further excluded those with major chronic conditions (e.g., cancer, high blood pressure, cardiovascular disease, and other comorbidities), the adjusted HR was 1.92 (95% CI 1.03-3.56; p 5 0.04). The interactions between RLS and other risk factors (older age, overweight, short sleep duration, smoking, low physical activity, and unhealthy diet) in relation to total mortality riskwere not significant (p for interaction .0.2 for all). Conclusion: We observed that men with RLS had a higher overall mortality and this association was independent of known risk factors. The increased mortality in RLS was more frequently associated with respiratory disease, endocrine disease, nutritional/metabolic disease, and immunologic disorders. Future research exploring the pathophysiologic relationship between these disorders and RLS is warranted. © 2013 American Academy of Neurology.
Han X.,Tianjin First Central Hospital
Zhonghua zhong liu za zhi [Chinese journal of oncology] | Year: 2013
To investigate the effect of demethylating agent 5-aza-2'-deoxycytidine (5-Aza-CdR) on the growth of human pancreatic cancer cell line MiaPaca2 and the expression and methylation of tumor suppressor gene RUNX3. Human pancreatic cancer cell line MiaPaca2 cells were treated with different concentrations of 5-Aza-CdR. Morphological changes of MiaPaca2 cells were observed by light microscopy. The activity of cell proliferation was analyzed by MTT assay. The changes of RUNX3 mRNA expression were detected by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR). Changes of RUNX3 gene methylation was detected by methylation-specific polymerase chain reaction. MiaPaca2 cells were treated with 2.5, 5, 10 and 20 μmo1/L 5-Aza-CdR, respectively. The inhibition rates of MiaPaca2 cells treated for 24 h were (9.17 ± 2.15)%, (10.75 ± 2.04)%, (12.57 ± 1.64)% and (18.70 ± 1.51)%, respectively. The inhibition rates were (14.94 ± 1.68)%, (18.60 ± 1.57)%, (22.84 ± 1.58)% and (33.24 ± 1.53)%, respectively, after 48 h treatment; (21.46 ± 1.60)%, (28.62 ± 1.72)%, (35.14 ± 1.64)% and (45.06 ± 1.47)%, respectively, after 72 h treatment; and (26.35 ± 1.71)%, (34.48 ± 1.69)%, (40.05 ± 1.60)% and (49.99 ± 1.61)%, respectively, after 96 h treatment. The differences between inhibition rates of each experimental and control groups (0.00 ± 0.00)% were statistically significant (P < 0.05). At the same time, the inhibition rates of different concentration groups showed significant differences (P < 0.05). At 48 h, 72 h and 96 h, the inhibition rates of each pair concentration groups showed significant differences (P < 0.05). 5-Aza- CdR inhibited the growth of MiaPaca2 cells, and the higher the concentration, the stronger the inhibition after 24 h. 5-Aza-CdR also reversed the methylation status of RUNX3 gene, and restored the expression of RUNX3 mRNA with a dose-effect relationship. The methylation of RUNX3 gene is significantly related with the occurrence and development of pancreatic cancer, and abnormal methylation of RUNX3 gene may contribute to the loss of RUNX3 mRNA expression. 5-Aza-CdR may effectively cause reversion of RUNX3 methylation, and treatment with 5-Aza-CdR can reactivate the gene expression and inhibit the cell growth. This may provide a new way for diagnosis and treatment of pancreatic cancer.