ABSTRACT
Objective To explore the feasibility of low-concentration contrast agent and low-dose technology for pulmonary angiography by comparing the image quality and radiation doses to the patient by different tube voltages and concentrations of contrast agents.Methods Totally 60 patients suspected with pulmonary embolism were divided into C, L1 and L2 groups, of which,Group C had the scanning parameters of 120 kV and 350 mgI/ml,Group L1 had the parameters as 100 kV and 350 mgI/ml and Group L2 had the parameters of 100 kV and 270 mgI/ml.The three groups had the tube voltage as 500 mA, the contrast agent dose as 25 ml,physiological saline dose as 40 ml and flow rate as 4.5 ml/s.SPSS 19.0 software was used to compare and analyze the CT values of pulmonary artery segment,superior vena cava and ascending aorta,main pulmonary artery noises,the image quality as well as the radiation doses of volume scanning. Results The three groups had the main pulmonary aortas and their branches display clearly to meet clinical requirements.When compared with Group C,Group L1 had higher CT values of the main pulmonary aorta and its branches,higher image noise while lower radiation dose (P<0.01);Group L2 had equivalent CT values of the main pulmonary aorta and its branches (P>0.05),higher image noise while lower radiation dose (P<0.01).When compared with Group L1,Group L2 had lower CT values of the main pulmonary aorta and its branches (P<0.01),and equivalent image noise and radiation dose (P>0.05).Conclusion Low-concentration contrast agent and low-dose technology gains feasibility and advantages when used in 320-slice CT pulmonary angiography.
ABSTRACT
Bronchial asthma is a chronic airway allergy disease involving the imbalance of Th1/Th2. Th2 shift is one of the primary causes of asthma. Recent studies have found that T cell immunoglobulin and mucin domain molecule 1 (TIM-1) play important roles in T cell activation and Th1/Th2 differentiation in asthma, which has been intensively reported in recent researches. This article reviews the characteristics of TIM-1 gene and its role in the pathogenesis of bronchial asthma.
ABSTRACT
Objective To investigate the effect of T cell Ig and mucin 1 (TIM-1) on MUC5AC and Th2 cytokine expression in the airway of asthmatic mice, so as to understand the mechanism of airway mucus hypersecretion. Methods Thirty healthy female C57BL/6 mice were randomly divided into control,asthmatic and TIM-1 mAb treated groups, with 10 mice in each group. The proportion of TIM-1 positive cells in peripheral blood mononuclear cells (PBMCs), MUC5AC mRNA expression in the airway, levels of IL-13, IL-4 and IL-5 in bronchoalveolar lavage fluid (BALF), and the number and volume of airway mucous cells were examined in the three groups. Results The proportions of PBMCs TIM-1 positive cells in asthmaticGl. 20%) and TIM-1 mAb treated (5. 11%) mice were significantly higher than that in the control group (0. 64%, P<0. 05), and that in TIM-1 mAb treated mice was significantly lower than that in the asthmatic mice (P<0. 05). (2) MUC5AC mRNA expression in the airway mucous cells in the asthmatic (17. 3 + 1. 4) and TIM-1 mAb treated (5. 6 + 0. 3) mice were significantly higher than that in control mice (P<0. 05). The BALF levels of IL-13 (ng/ml), IL-4 (pg/ml), and IL-5 (pg/ml) were 16. 80 ±0. 63, 614. 72 + 117. 39, and 1 681. 13 + 613.55 in the asthmatic, and were 5. 70 ± 0. 64, 325. 78 ± 86. 54, and 513. 42 + 86. 87 in TIM-1 mAb treated mice, respectively, which were all significantly higher than those in the control mice ([1. 09 + 0. 25] ng/ml for IL-13, [17. 56 + 3. 01] pg/ml for IL-4, and [30. 78 + 9. 67] pg/ml for IL-5, P<0. 05). And all the above parameters in the TIM-1 mAb treated mice were significantly lower than those in the asthmatic mice (P
ABSTRACT
Bronchial asthma is a chronic airway allergy disease involving the imbalance of Th1/Th2. Th2 shift is one of the primary causes of asthma. Recent studies have found that T cell immunoglobulin and mucin domain molecule 1 (TIM-1) play important roles in T cell activation and Th1/Th2 differentiation in asthma, which has been intensively reported in recent researches. This article reviews the characteristics of TIM-1 gene and its role in the pathogenesis of bronchial asthma.
ABSTRACT
The aim of the present study was to explore the effect of nitric oxide (NO) on iron-induced toxicity in rat hearts. Langendorff perfused rat heart and enzymatically isolated cardiomyocytes were used. It was shown that lipophilic Fe-HQ reduced the contractile amplitude, velocity and end-diastolic cell length in the cardiomyocyte, while the left ventricular developed pressure (LVDP), +/-dp/dt(max), heart rate and coronary flow showed biphasic alterations, which increased in the first 2 min and then was followed by a decline in isolated perfused rat heart; the contents of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary effluent and the malondialdehyde (MDA) in the myocardium were increased. L-arginine (L-Arg), an NO precursor, reduced the contractile amplitude and end-diastolic cell length in the cardiomyocyte; but reversibly increased LVDP, +/-dp/dt(max), and coronary flow in isolated perfused rat heart. Pretreatment with L-Arg aggravated the Fe-HQ-induced decrease in contractile amplitude, velocity and end-diastolic cell length in the cardiomyocyte; LVDP, +/-dp/dt(max), heart rate and coronary flow were significantly reduced in the perfused heart, and the levels of LDH and CK increased in the coronary effluent. In contrast, the NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) blocked the Fe-HQ induced change in contractile amplitude, velocity and end-diastolic cell length in the cardio- myocyte; it inhibited the decrease in LVDP, LVEDP and +/-dp/dt(max), and reduced the LDH and CK. Removing endothelial cells in coronary vessels attenuated the increase in LVDP and +/-dp/dt(max) at the beginning of Fe-HQ perfusion. It is suggested that L-Arg aggravates the iron-induced cardiac dysfunction, NO can mediate the iron-induced toxicity in heart, and endothelial cells in coronary vessels play an important role in the early stage of the effect of iron.