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Objective:To investigate the ethics and existing problems of experimental animals in medical experiments and experimental teaching, and to formulate countermeasures so that animal ethics and animal welfare can be truly reflected in medical experiments.Methods:In this study, a "Basic Function Experiment Center Animal Experiment Questionnaire" with 25 questions was formulated from three aspects: the ethical cognition of experimental animals, whether animal experiments are ethical or not, how to view the problems of animal ethics and experimental teaching and the cognition of virtual simulation experiment teaching. Questionnaire was sent to Hubei University of Medicine to investigate the international students of Batch 2017 (5-year program), undergraduates of Batch 2017 (5-year program) and nursing students of Batch 2018 (4-year program) as well as teachers, researchers and employees of laboratory animal center (all with bachelor degree or above). The survey results were expressed as percentage.Results:The recovery rate of the questionnaire in this study was 98.04%(2 451/2 500), among which the practitioners, teachers and researchers in the laboratory animal center clearly understood the ethics of experimental animals, but there was a widespread phenomenon of lagging ethics among the students. For example, 16.24% (398/2 451) students had not received animal experiment ethics education and training, 29.46% (722/2 451) were not clear about animal protection laws and regulations, 7.14% (175/2 451) thought animal experiments were immoral; 29.54% (724/2 451) had vague cognition of animal welfare and ethical knowledge; 25.91% (635/2 451) were not familiar with the operation steps; 9.38% (230/2 451) were indifferent to the extra treatment of animals due to operation errors, 7.83% (192/2 451) chose to give up the experiment in the treatment of animals after massive bleeding, only 5.43% (133/2 451) chose to continue the experiment after timely hemostasis and infusion, and 9.26% (227/2 451) chose to do operations unrelated to the experiment. After the experiment, 2.28% (56/2 451) chose to kill the animals by bloodletting, only 5.51% (135/2 451) chose excessive anesthesia euthanasia, and 1.96% (48/2 451) chose to kill the animals by cervical dislocation and violence. Only 15.79% (387/2 451) chose to remember the dead animal for 2 minutes. Only 32.56%(798/2 451) of the respondents understood virtual simulation experiment, 34.92% (856/2 451) of the respondents thought that virtual simulation experiment or experimental teaching video could be used to replace the existing live animal experiment, 77.56% (1 901/2 451) believed that the construction of virtual simulation laboratory should be strengthened.Conclusion:It is imperative to strengthen the education of students' ethics of experimental animals, which is conducive to the establishment of correct ethics of experimental animals for medical students, so that the "3R" principle and animal welfare can be truly implemented in experimental teaching and scientific research experiments.
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To study the mechanism of injection of sinomenine (Sinomenine,SIN)into Jiaji point in the treatment of L1-L5 segment Compression of fracture spine (VCF) in rabbits.Methods:54 rabbits were randomly divided into blank control group,model group and sinomenine group (group SIN)by the random number table.All the 2 groups established L1-L5 segment VCF model except the blank control group.After molding,the SIN group was injected SIN at both sides of the L1-L5 section of the vertebral column,the model group and the blank control group were injected the same volume of physiological saline as comparison.The 3 groups were treated for 4 weeks.Fracture of vertebral bone growth differentiation factor 2 (Growth differentiation,FACTOR2,GDF2),vascular endothelial growth factor (Vascular endothelial,growth factor,VEGF) and the expression of VEGF-mRNA were determined by immunohistochemical staining method;in venous blood,activities of nitric oxide (Nitric oxide NO),super oxide dissuade (Super oxide dims,unties,SOD) and bone protection Su (OPG) were detected by ELISA;immunofluorescence was used to measure two chitosan,image analysis method was used to detect spinal bone density in L1-L5 segment,the ELISA was used to detect inflammatory factor interleukin 1 beta (IL-1 beta),IL-6 beta,beta IL-17 in the spinal disc.Results:compared with the model group,in the SIN group,VEGF,VEGFmRNA and GDF2 in L1-L5 segment of spine were highly expressed,and the bone density increased (P＜0.05);two chitosan in intervertebral disc increased,IL-1beta,IL-6 beta,IL-17 beta,(P＜ 0.05);NO in venous blood decreased OPG,SOD increased (P＜0.05),the differences were statistically significant.Conclusion:injection of SIN into Jiaji can promote the healing of VCF in L1-L5 segment in rabbits.
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Objective To examine whether the two vascular paracrine/autocrine factors, angiotensin Ⅱ (Ang Ⅱ) and endothelin, participate in the pathogenesis of arterial calcification. Methods Nicotine and vitamin D3 treated rats were studied. Vascular calcification was confirmed by using Von Kossa staining, measurement of calcium content,45Ca2+ uptake assay and alkaline phosphatase (ALP) activity. The plasma and vascular Ang Ⅱ and endothelin levels were measured by using radioimmunoassay. Angiotensinogen and endothelin mRNA levels were determined by RTPCR. Results The arterial calcium content, 45Ca2+ uptake and ALP activity were increased in calcification groups compared with control ( P ＜ 0.01 ). Administration of the angiotensin receptor antagonist losartan, the endothelin receptor antagonist bosentan, and the angiotensin-converting enzyme inhibitor captopril reduced significantly the arterial calcium content, 45Ca2+ uptake and ALP activity. In addition, the plasma and aortic Ang Ⅱ and endothelin contents, and vascular angiotensinogen and endothelin mRNA expression were significantly up-regulated ( P ＜0.05).Conclusions These findings suggest that functional renin-angiotensin system and endothelin pathway are involved in vascular calcification, and that activation of these systems could potentiate pathogenesis of arterial calcification. ( J Geriatr Cardiol 2004;1(2) :108-113. )
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Objective To explore the effect of intra-and post-operative administration of supplemental high concentration oxygen on abdominal clean-contaminated surgical wound infection.Methods From January 2001 to June 2005, 425 patients undergoing abdominal clean-contaminated operation were randomly divided into receive FiO2 60 % (n=213, study group) or FiO2 28 % (n=212, control group) inspired oxygen during the operation and two hours postoperatively. The partial pressure of oxygen in arterial blood and the peripheral arterial oxygen saturation was were measured two hours after operation. During 15 postoperative days, the wounds that drained pus were considered infected.Results The results showed that the partial pressure of oxygen in arterial blood was significantly higher in the study group than in the control group (P
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AIM: To observe the changes of cystathionine-lyase/hydrogen sulfide(CSE/H_2S) in vivo in vascular calcification and to explore the role of CSE/H_2S in vascular calcification.METHODS: Vascular calcification model in rats was induced by administration of vitamin D_3 plus nicotine.The extent of calcification was estimated by assaying calcium content.[~(45)Ca~(2+)] deposition and alkaline phosphatase(ALP) activity were detected.CSE mRNA amount was determined by using competitive quantitative RT-PCR.The content of H_2S and activity of CSE in the plasma and cardiovascular tissues were also determined with biochemical methods.RESULTS: Calcium content in myocardium increased by 3.8 folds in a calcification model.Compared to control,calcium content,[~(45)Ca~(2+)] accumulation and ALP activity in calcified arteries increased by 6.8,1.4,and 1.9 folds,respectively(P
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AIM: To explore the effects of angiotensin II on aortic calcification in the rat. METHODS: Arterial calcification of Sprague-Dawley rats was induced by vitamin D_3 plus nicotine. Calcification was confirmed by Von Kossa staining, measurement of calcium content, [~(45)Ca~(2+)] accumulation and alkaline phosphatase (ALP) activity of vascular tissue. RESULTS: The results showed that calcium content, [~(45)Ca~(2+)] accumulation and ALP activity in calcified arteries increased significantly compared with those of control. Ang Ⅱ levels in plasma and aortic tissues and the amount of angiotensinogen mRNA in calcified aorta were also increased as compared with control. Captopril (inhibitor of ACE) and losartan (Ang Ⅱ receptor inhibitor) decreased significantly the content of calcium, [~(45)Ca~(2+)] uptake and ALP activity in calcified aorta. Ang Ⅱ levels in plasma and aortic tissues and the amount of angiotensinogen mRNA in aortic tissue were down-regulated by captopril. The amount of angiotensinogen mRNA and the content of Ang Ⅱ in the calcified aorta were also decreased by losartan. CONCLUSION: The captopril and losartan significantly alleviate the vascular calcification. [
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AIM: To investigate the change of heme oxygenase (HO)-carbon monoxide (CO)-cyclic guanosine monophosphate (cGMP) pathway in vascular calcification, to clarify the cellular and molecular mechanimsm in vascular calcification.METHODS: Vascular calcification model was established in rats by using vitamin D 3 and nicotine. The relative content of HO-1 mRNA, immunochemistry (IH) for HO-1, HO activity, HbCO formation and content of cGMP in aorta were measured. RESULTS: Compared to those of control rats, the HO-1 mRNA level in vessels of rats in VDN group(vascular calcification group) were decreased by 34.9% ( P
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AIM: To study alterations of nitric oxide synthase (NOS) in cardiac sarcop lasmic reticulum from rats with myocardial calcification, and to explore the mec hanism of inhibition of SR function in the rats with myocardial calcification. METHODS: The myocardial calcification rat models were prepared by vit amin D3 plus nicotine for 2 weeks and 6 weeks. Cardiac SR was separated by centrifugating. T he nitric oxide (NO) production, NOS activity and NOS protein expression in the SR were perfor med. RESULTS: Compared with control, myocardial calcium content in t he 6 weeks i ncreased by 408%(P