Objective To study the window technique in evaluating the chronic obstructive emphysema and pulmonary residual volume in long-term smoker without symptoms.Methods 50 cases with chronic obstructive emphysema proved clinically,50 long-term smokers were undergone spiral CT scan of chest and compared with 30 health volunteer,the images were designed using the mean CT value in smoking group as window level and two times of ?2 as window width.Results The white imaging was appeared in the most of the group of volunteer,the images were dark on different degree in group one,while the images were as ground glass on different degree in group two.Conclusion This window technique is helpful in evaluating the chronic obstructive emphysema and residual volume of lung in long-term smoker

Objective To observe the effect of tanshinone IIA on the myocardial calmodulin (CaM) and calmodulin dependent protein kinase II (CaMK) mRNA expression and heart function of acute myocardial infarction rats. Methods A total of 100 rats were randomly divided into the sham operation group, the model group, and the tanshinone ⅡA group. The model of acute myocardial infarction was established by the ligation of left anterior descending coronary artery ligation with 45 min, and reperfusion with 45 min, and the above process was repeated 3 times. Tanshinone IIA group was treated with intravenous injection of 10 mg/kg sodium tanshinone ⅡA, while the sham operation group and the model group with 10 mg/kg saline, and all treatment last 7 days. The mRNA expressions of CaM and CaMKII were determined. TTC staining was used to observe areas of myocardial infarction. The left ventricular maximum rise/fall rate (±LVdp/dtmax), myocardial contraction tension, heart rate and heart function index were detected pre-and post-treatment by the Langendorff device perfusion of isolated heart. Results Compared with the model group, the mRNA expression of and CaM mRNA (1.29 ± 0.19 vs. 2.31 ± 0.21) and CaMK II (1.10 ± 0.07 vs. 2.13 ± 0.18) in the tanshinone IIA group were significantly lower (P<0.05), and the areas of myocardial infarction (25.12%± 0.43%vs. 35.15%± 0.64%) significantly decreased (P<0.05), and the IT (2.03 ± 0.14 g vs. 1.06 ± 0.12 g), the ±LV dp/dtmax (4 701.2 ± 135.3 mmHg/s vs. 3 214.7 ± 110.2 mmHg/s, 2 518.7 ± 65.4 mmHg/s vs.1 960.3 ± 62.5 mmHg/s) significantly increased (P<0.05). Conclusion Tanshinone IIA may protect myocardial ischemia by regulating the mRNA expression of CaM and CaMKⅡ.

Liver fibrosis is a key pathological process in the progression of chronic liver disease to cirrhosis and even liver cancer.The occurrence of liver fibrosis is a highly integrated and dynamic pathological process result ing from the interactions of many cells and cytokines.The Notch signaling pathway is an evolutionarily conserved intercellular signal transduction mechanism that plays important roles in regulating the development and tissue renewal of multicellular animals.Multiple studies have shown that Notch signal transduction participates in the formation of liver fibrosis in a variety of ways.Therefore,this paper reviews the role of Notch signaling in cells involved in the formation of liver fibrosis to explain the function of this signaling pathway in liver fibrosis.