Establishment of Rabbit Abdominal Aortic Atherosclerosis Model by Pancreatic Elastase Infiltration Associated with High Fat Diet.

BACKGROUND: The aim of this study was to evaluate the feasibility of a high fat diet (HFD) associated with pancreatic elastase (PE) infiltration, in establishing the rabbit aortic atherosclerosis model. METHODS: The HFD+PE method and the HFD+saccule injury (SI) method were simultaneously used to prepare the rabbit atherosclerosis model; the control group was established with the normal diet. Biochemical indicators, radiological imaging, pathomorphology and immunohistochemistry were used to evaluate the HFD+PE modeling results. RESULTS: There were significant changes in the blood lipid contents, as well as the pathomorphological and immunohistochemical results between the two experimental groups and the control group (p < 0.05). However, there was no difference between the two experimental groups. The rabbit aortic atherosclerosis model prepared by the HFD+PE method had no significant difference in the local vascular pathomorphological and immunohistochemical results with the traditional HFD+SI method. CONCLUSIONS: The use of HFD with PE infiltration is feasible in establishing the rabbit aortic atherosclerosis model. KEY WORDS: Animal model; Atherosclerosis; Rabbit.

Effects of iodinated contrast agents on renal oxygenation level determined by blood oxygenation level dependent magnetic resonance imaging in rabbit models of type 1 and type 2 diabetic nephropathy.

BACKGROUND: To evaluate the effects of contrast agents containing increasing concentrations of iodine on the renal oxygenation level determined by blood oxygenation level dependent (BOLD) magnetic resonance imaging (MRI) in a rabbit model of diabetic nephropathy. METHODS: BOLD-MRI was performed using saline or iodinated (I) contrast agents (200, 240, 300, 350 and 400 mg I/mL) at 1, 24, 48, and 72 h after experimentally inducing type 2 diabetic nephropathy in rabbits. Differences in renal oxygenation levels between type 1 and type 2 diabetic nephropathy were also assessed by BOLD-MRI after injecting 400 mg I/mL of contrast agent. RESULTS: Contrast agents increased the R2* values of the renal cortex, outer medulla, and inner medulla to the maximum levels at 24 h. The R2* values then decreased to their lowest levels at 72 h. The R2* was highest following injection of 400 mg I/mL, especially in the outer medulla. The R2* values were not significantly different between types 1 and 2 diabetic nephropathy. CONCLUSIONS: Iodinated contrast agents had the greatest influence on renal outer medulla oxygenation level at 24 h in type 2 diabetic nephropathy, with the greatest effects observed at the 400 mg I/mL dose level. There were no differences in BOLD-MRI values between type 1 and type 2 diabetic nephropathy after administering the contrast agent at 400 mg I/mL.

Budd-Chiari syndrome in China: A 30-year retrospective study on survival from a single center.

AIM: To investigate 30-year treatment outcomes associated with Budd-Chiari syndrome (BCS) at a tertiary hospital in China. METHODS: A total of 256 patients diagnosed with primary BCS at our tertiary hospital between November 1983 and September 2013 were followed and retrospectively studied. Cumulative survival rates and cumulative mortality rates of major causes were calculated by Kaplan-Meier analysis, and the independent predictors of survival were identified using a Cox regression model. RESULTS: Thirty-four patients were untreated; however, 222 patients were treated by medicine, surgery, or interventional radiology. Forty-four patients were lost to follow-up; however, 212 patients were followed, 67 of whom died. The symptom remission rates of treated and untreated patients were 81.1% (107/132) and 46.2% (6/13), respectively (P = 0.009). The cumulative 1-, 5-, 10-, 20-, and 30-year survival rates of the treated patients were 93.5%, 81.6%, 75.2%, 64.7%, and 58.2%, respectively; however, the 1-, 5-, 10-, 20-, and 30-year survival rates of the untreated patients were 70.8%, 70.8%, 53.1%, 0%, and unavailable, respectively (P = 0.007). Independent predictors of survival for treated patients were gastroesophageal variceal bleeding (HR = 3.043, 95%CI: 1.363-6.791, P = 0.007) and restenosis (HR = 4.610, 95%CI: 1.916-11.091, P = 0.001). The cumulative 1-, 5-, 10-, 20-, and 30-year mortality rates for hepatocellular carcinoma were 0%, 2.6%, 3.5%, 8%, and 17.4%, respectively. CONCLUSION: Long-term survival is satisfactory for treated Chinese patients with BCS. Hepatocellular carcinoma is a chronic complication and should be monitored with long-term follow-up.

Mig-6 overcomes gefitinib resistance by inhibiting EGFR/ERK pathway in non-small cell lung cancer cell lines.

Non small cell lung cancer (NSCLC) accounts for 85% of all lung cancers and is the most common cause of lung cancer death. Currently, the epidermal growth factor receptor inhibitor gefitinib is widely used for patients with advanced NSCLC. However, drug resistance is a major obstacle. Mig-6 is a feedback inhibitor of EGFR and its down-stream pathway; it has been shown to play a role in gefitinib sensitivity. There is neither systematical research on the relationship between Mig-6 expression and gefitinib sensitivity, nor has the contribution of up-regulated Mig-6 on the gefitinib-resistant cell lines. In the present work, four NSCLC cell lines (H1299, A549, PC-9, and PC-9/AB11) with different sensitivities to gefitinib were subjected to analysis of the expression of Mig-6. We found that Mig-6 is over-expressed in gefitinib-sensitive NSCLC cell lines, but is low in gefitinib-resistant NSCLC cell lines. Further analysis revealed that over-expression of Mig-6 increased cell apoptosis and inhibited proliferation of gefitinib-resistant NSCLC cells treated with gefitinib, whereas lowering the expression of Mig-6 decreased cell apoptosis and promoted cell proliferation after treatment with gefitinib in gefitinib-sensitive NSCLC cell lines. These results suggest that Mig-6 is involved in mediating the response to gefitinib in NSCLC cell lines. Additionally we demonstrated that Mig-6 could reverse gefitinib resistance through inhibition of EGFR/ERK pathway in NSCLC cells. Our work uncovered that Mig-6 may be an effective therapeutic target in gefitinib-resistant lung cancer patients.