[Establishment of acute pulmonary edema model induced by high concentrations of nitrogen dioxide in rats].

OBJECTIVE: To establish the rats model of acute pulmonary edema induced by inhalation of high concentrations of nitrogen dioxide (NO2). METHODS: 38 SD rats were divided into the experimental group (n = 30) and the control group (n = 8). 30 rats in the experimental group were exposed to (6747.47 ± 25.24) mg/m(3) NO2 in the exposure system. At the time point of 6, 12, 18, 24 h, chest X-ray examination was taken for the experimental group. And at each time point, 6 rats were sacrificed after taking blood samples. After sacrificing, the lung of rats was taken for pathological examination and calculated lung wet/dry weight ratio. Erythrocyte superoxide dismutase (SOD) activity and plasma atrial natriuretic peptide (ANP) concentration of blood samples were detected. RESULTS: Acute pulmonary edema was successfully induced by exposure to NO2 in 30 rats within 24 hours. There were some cloudy shadows without clear edge on the chest X-ray. To the time point of 12 hours, shadows combined with each other, and to the time point of 18 hours, the whole lung became "white" on the X-ray. The situation stabilized but not improved at the time point of 24 hours. HE staining of the lung tissue showed that to the time point of 6 hours, the alveolar gap increased and small amount of eosinophilic liquid leaked into alveolar. To the time point of 12 hours, alveolar combined with each other and eosinophilic liquid increased in amount. To the time point of 18 hours, the whole alveolar was filled with eosinophilic liquid and the situation stabilized till the time point of 24 hours. Wet/dry weight ratio of the experimental group at each time point were 5.6 ± 0.20, 6.89 ± 0.25, 8.03 ± 0.47, 7.81 ± 0.45. There was significant difference compared with the control group which was 4.72 ± 0.06 (P < 0.01). There was statistical difference between 12, 18, 24 h and 6 h time points (P < 0.01). Moreover, statistical difference was observed between 18, 24 h and 12 h time points for wet/dry weight ratio (P < 0.01). The erythrocyte SOD activity reduced significantly. Compared with the control group, there was a statistical difference (P < 0.01) at each time point. After exposure of 18 and 24 hours, plasma ANP concentration (136.66 ± 35.37) and (134.10 ± 60.41) ng/ml respectively, which were higher than (31.31 ± 13.06) ng/ml of control group and (34.71 ± 13.42) ng/ml of 6 hours time point and (47.98 ± 7.86) ng/ml. The differences were significant (P < 0.01). CONCLUSION: High concentrations of NO2 can induce acute pulmonary edema model successfully in SD rats.

Severe cutaneous adverse drug reaction to leflunomide: a report of two cases.

The purpose of this study was to report severe cutaneous reactions in two patients related with leflunomide. A 13-year-old girl was treated with leflunomide for systemic lupus erythematosus. Three months later a progressive generalized blistering formation occurred and epidermolysis appeared on her skin. Methylprednisolone pulse therapy and intravenous immunoglobulin were used to control the severe cutaneous reactions. The patient recovered within 18 days. Another case is a 63-year-old woman who was treated with leflunomide for primary Sjögren's syndrome. Four months later widespread prunosus skin rash appeared on her skin. Methylprednisolone pulse therapy was also used to control the severe cutaneous reactions. The patient was recovered 11 days later. Our report suggests that an association between leflunomide intake and severe cutaneous reactions in rheumatic disease patients should be considered.

Severe keloids caused by hydrogen cyanide injury: a case report.

The purpose of this study was to report severe keloids caused by hydrogen cyanide injury. Hydrogen cyanide poisoning is still a problem as an occupational disease in China. We report a 37-year-old man with severe hydrogen cyanide poisoning. The patient fell on the floor after inhalation of hydrogen cyanide and was burned on his back by hydrocyanic acid. Sequential treatment included amyl nitrite by inhalation, intravenous sodium nitrite 3%, and intravenous sodium thiosulfate 25%. Other treatment consisted of incision of the trachea, mannitol and furosemide, antibiotics, and nutrient support measures. The patient also received hyperbaric oxygen therapy; during the first treatment, he became apneic and cardiopulmonary resuscitation was supplied in the hyperbaric oxygen chamber. He eventually recovered, but a large amount of keloids developed on his back and buttocks.

[Clinical observation of rheumatoid arthritis associated interstitial lung disease patients and changes of serum cytokines thereof].

OBJECTIVE: To observe the clinical feature of rheumatoid arthritis associated interstitial lung disease (RA-ILD) patients and changes of serum cytokines tumor growth factor (TGF)-beta 1, tumor necrosis factor (TNF)-alpha, insulin-like growth factor (IGF)-1, and platelet derived growth factor (PDGF)-AB. METHODS: The clinical manifestations, lung high resolution CT (HRCT), lung functions, blood gas and other relative laboratory findings of 30 RA-ILD patients and 35 RA patients were observed. ELISA was used to detect the levels of TGF-beta 1, TNF-alpha, IGF-1, and PDGF-AB. Thirty healthy volunteers were observed too as controls. RESULTS: The clinical manifestations of RA-ILD patients were more serious than those of the RA patients. The ESR was faster, the serum C-reactive protein, rheumatoid factor (RF), and globulin levels higher, and pulmonary arterial pressure higher too in the RA-ILD patients than in the RA patients (all P<0.01). The main respiratory manifestations of the RA-ILD patients were cough, expectoration, chest distress, short breath, chest pain, change of breath sounds, Velcro râles, and dyspnea. The main lung HRCT findings included thickening of interlobular septum and bronchial wall, pachynsis pleurae, mosaic sign, bronchiectasis, emphysema, patching shadow, honeycombing, fibrous scar, etc. Pulmonary function test showed that the levels of vital capacity, forced vital capacity, maximum midexpiratory flow, and diffusing capacity of the lung for carbon monoxide of the RA-ILD patients were all significantly lower than those of the RA patients (all P<0.01). Arterial gas test showed that the PO2 of the RA-ILD patients was significantly lower than that of the RA patients (P<0.01). The TGF-beta 1; TNF-alpha, IGF-1, and PDGF-AB of both the RA-ILD and RA patients were all significantly higher than those of the healthy volunteers (all P<0.01), and the levels of these cytokines of the RA-ILD patients were all higher than those of the RA patients (all P<0.01). CONCLUSION: The symptoms and signs of the RA-ILD patients are more serious, the lung HRCT changes more obvious, lung function decreases, and the levels of TGF-beta 1, TNF-alpha, IGF-1, and PDGF-AB increase.

[Clinical study on treatment of acute paraquat poisoning].

OBJECTIVE: To investigate the clinical therapeutic effect of methylprednisolone combined with cyclophosphamide and Etanercept method on acute paraquat poisoning. METHODS: 136 patients with acute paraquat poisoning were divided into the normal therapy group and the intensive therapy group randomly. Methylprednisolone, cyclophosphamide and Etanercept were used in the intensive therapy group. Methylprednisolone 500 mg was given intravenously per day for continuous three days followed by 200 mg intravenous per day. Then methylprednisolone was decreased gradually 14 d or 21 d later according to the patient's condition. Cyclophosphamide 600 mg was given intravenously twice weekly for 2 weeks and Etanercept 25 mg was given hypodermic injection twice weekly for 3 weeks. Curative effect evaluation was done at 7, 14, 21 d and 12 weeks after therapy. RESULTS: The survival rate of the intensive therapy group was obviously higher than that of the normal therapy group (P<0.01) on 7, 4, 21 d and 12 weeks. The cure rate of the intensive group were 94.6% (intake dose<50 ml 20% paraquat solution), 75.0% (intake dose 50 approximately 100 ml 20% paraquat solution), 12.5% (intake dose>100 ml 20% paraquat solution) respectively, while the cure rate of the normal group were 16.7% (intake dose<50 ml 20% paraquat solution), 8.3% (intake dose 50 approximately 100 ml 20% paraquat solution), 0% (intake dose>100 ml 20% paraquat solution) respectively. The total cure rate of the intensive therapy group (78.3%) 12 weeks later was higher than that of the normal group (11.9%). CONCLUSION: Methylprednisolone combined with cyclophosphamide and Etanercept intensive therapy has the curative effect on acute paraquat poisoning.

Surface acidity effects of Al-SBA-15 mesoporous materials on adsorptive desulfurization.

SBA-15 and Aluminum-substituted SBA-15 with Si/Al molar ratio 10 (Al-SBA-15(10)) mesoporous materials were directly synthesized by a hydrolysis approach and characterized by a powder X-ray diffraction (XRD), N2 physisorption analysis and Fourier transform infrared (FTIR) etc. The relative number of hydroxyl groups was investigated by in situ FTIR systematically. The acid type and acid strength of the adsorbents were monitord by FTIR at 423 K and 673 K, respectively, utilizing pyridine as a probe. Desulfurization performances of the adsorbents were investigated via static adsorption experiment. Gas chromatography-sulfur chemiluminescence detector (GC-SCD) was employed to detect the sulfur compounds in model fuels before and after treated by the adsorbents. The calcined Al-SBA-15(10) material shows well-ordered hexagonal mesostructure and strong Lewis acid sites (L acid) and weak Brönsted acid sites (B acid). The number of hydroxy on the surface of the Al-SBA-15(10) is more than that of SBA-15, which is beneficial to further modifications such as spontaneous monolayer dispersion. Desulfurization performance of the adsorbents is affected by surface acidity of adsorbents and the constituent of model fuels (olefins, arene, etc.). The thiophene and olefins adsorbed on the B acid site of the adsorbent may occur subsequently alkylation reactions, which may block the pores of the adsorbents and thus cause the reduction of desulfurization capacity.