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1.
Journal of Forensic Medicine ; (6): 85-87, 2009.
Article in Chinese | WPRIM | ID: wpr-983447

ABSTRACT

OBJECTIVE@#To investigate the expression changes of aquaporins 1 (AQP1) in contused lung tissue of rats and its relationship with pulmonary edema.@*METHODS@#SD rats were randomly divided into experimental and control groups. The pulmonary contusion models were then prepared. The expression and distribution of AQP1 in lung tissue of the rats were detected by immunohistochemistry.@*RESULTS@#The lung tissue showed edema, hemorrhage, inflammatory cell infiltration 1 h, 3 h after pulmonary contusion, and the inflammatory response aggravated after 5 h. AQP1 expression at 1 h, 3 h and 5 h in the contusion group were significantly higher than that of the control group (P < 0.01). The expression of AQP1 continued to increase with time and aggravation of edema compared to the control group. AQP1 was mainly distributed in the capillary endothelial cells and interstitial cells of the bronchial and alveolar walls. Although there were no observed changes in AQP1 expression location in contused lung tissue, the intergrated optical density(IOD) showed significant statistical difference (P < 0.01).@*CONCLUSION@#There might exist an dysregulation of AQPs gene expression in contused lung tissue, leading to a large number of abnormal transmembrane water transportation and abnormal water accumulation, which may be one of the reasons for pulmonary edema in contused lung tissue.


Subject(s)
Animals , Female , Male , Rats , Aquaporin 1/metabolism , Contusions/metabolism , Forensic Pathology , Lung Injury/metabolism , Pulmonary Edema/metabolism , Random Allocation , Rats, Sprague-Dawley
2.
Journal of Forensic Medicine ; (6): 330-332, 2006.
Article in Chinese | WPRIM | ID: wpr-983215

ABSTRACT

OBJECTIVE@#To observe pathological changes and apoptosis in rats myocardial cells after Macleaya cordata total alkaloids poisoning, and to provide some references for Macleaya cordata total alkaloids poisoning detection.@*METHODS@#An experimental model of Macleaya cordata total alkaloids poisoning was established, and the technology of TUNEL staining was used.The results were analyzed by computer image analysis competitive system.@*RESULTS@#Quantities of apoptosis in myocardial cells in poisoning groups were much more than those in the control groups at different tages (P<0.01). In addition the quantities of apoptosis were different after different poisoning duration.@*CONCLUSION@#Although clinical symptoms was not obvious and could not be detected by poison analysis. Pathological changes induced by Macleaya cordata total alkaloids could be found through the apoptosis detection.


Subject(s)
Animals , Female , Male , Rats , Acute Disease , Apoptosis/drug effects , Cell Count , Disease Models, Animal , Immunohistochemistry , In Situ Nick-End Labeling , Myocardium/pathology , Myocytes, Cardiac/drug effects , Papaveraceae/chemistry , Papaverine/poisoning , Random Allocation , Rats, Sprague-Dawley , Staining and Labeling , Time Factors
3.
Journal of Forensic Medicine ; (6): 15-17, 2006.
Article in Chinese | WPRIM | ID: wpr-983119

ABSTRACT

OBJECTIVE@#To find out the pathological change and the toxic mechanism of Chloranthus serratus Roem. et Schalt in mice.@*METHODS@#Mice were intoxicated by oral administration with extracts of Chloranthus serratus Roem. et Schalt followed by pathological, serum biochemical, and coagulation mechanism examination.@*RESULTS@#The LD50 in mice was 41.12 g/kg; All poisoned mice serum BUN and ALT increased markedly; Thrombocyte decreased and coagulation time increased; The organ index of liver, spleen and kidneys increased significantly; The cells of liver, kidney and heart were degeneration and necrosis, There were extensive hyperemia and hemorrhage in many organs.@*CONCLUSION@#The experiment suggests that the target organs were liver, kidney, heart and blood vessels; The toxic mechanism was the damage on the mitochondrional, endoplasmic reticulum and coagulation system.


Subject(s)
Animals , Female , Male , Mice , Biomarkers/blood , Dose-Response Relationship, Drug , Endoplasmic Reticulum/drug effects , Forensic Pathology , Kidney/pathology , Lethal Dose 50 , Liver/pathology , Magnoliopsida/chemistry , Mitochondria, Heart/drug effects , Mitochondria, Liver/drug effects , Myocardium/pathology , Plant Extracts/toxicity , Random Allocation
4.
Journal of Forensic Medicine ; (6): 12-14, 2006.
Article in Chinese | WPRIM | ID: wpr-983118

ABSTRACT

OBJECTIVE@#In order to improve the accuracy and reliability in sudden cardiac death, the pathogenesis and relationship between the viral myocarditis and dilated cardiomyopathy were investigated.@*METHODS@#Improved immunohistochemical technique was adopted to detect the expression of the dystrophin in myocardium from 25 viral myocarditis, 28 dilated cardiomyopathy and 17 control cases including normal, coronary atherosclerotic heart disease and hypertension heart disease as control.@*RESULTS@#The positive rate of dystrophin protein expression in control group was 100%, that in viral myocarditis was 88%, and that in dilated cardiomyopathy was 57%, There were significant differences among three groups (P<0.05), and the correlation between viral myocarditis and dilated cardiomyopathy group (r = -0.526)were also found.@*CONCLUSION@#The myocardial cytoskeletal protein is disrupted in viral myocarditis and dilated cardiomyopathy, and the dystrophin protein may be involved in the pathogenesis of viral myocarditis and dilated cardiomyopathy. The viral infect and impair heart functions by cleaving host dystrophin proteins may ultimately contributes to the viral myocarditis to the converting from dilated cardiomyopathy.


Subject(s)
Female , Humans , Male , Cardiomyopathy, Dilated/metabolism , Case-Control Studies , Death, Sudden, Cardiac , Dystrophin/metabolism , Enterovirus Infections/complications , Immunohistochemistry , Myocarditis/virology , Myocardium/pathology , Staining and Labeling
5.
Journal of Forensic Medicine ; (6): 81-83, 2003.
Article in Chinese | WPRIM | ID: wpr-982976

ABSTRACT

OBJECTIVE@#To study the pathological change and the toxic mechanism of Dioscorea bulbifera L in mice.@*METHODS@#Sixty ICR mice were randomly assigned to four groups poisoned respectively with 200% Dioscorea bulbifera L of 1/4 LD50, 1/10LD50, 1/30LD50 and a control group treated with distilled water by oral administration. All animals were pathologically examined with LM and some of them were examined with TEM when the mice died during the experiment or the survival mice were sacrificed after thirty days.@*RESULTS@#The pathological changes showed fatty change and the increasing glycogen of liver cells; degeneration and necrosis of the epithelia of uriniferous tubules. The serum BUN and ALT of the experimental groups mice were higher than that of control group. Enzyme histochemical staining showed the decreasing activity of G-6-P and SDH in the liver cells in the experimental groups.@*CONCLUSION@#The experiment suggests that the target organs were liver and kidney. The toxic mechanism of Dioscorea bublifera L was the damage of the mitochondrional and endoplasmic reticulum membrane directly. As a result, the activity of the SDH and G-6-P decreased, the metabolism was affected.


Subject(s)
Animals , Female , Male , Mice , Chemical and Drug Induced Liver Injury/pathology , Dioscorea/toxicity , Endoplasmic Reticulum/pathology , Forensic Medicine , Kidney/pathology , Mice, Inbred ICR , Mitochondria, Liver/pathology , Random Allocation
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