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Objective@#To investigate the feasibility of echocardiography-guided closed-chest repeated intraventricular blood sampling in mice, and to clarify the maximum blood volume that can be collected by this method, and whether the method can be used for long-term repeated blood collection in mice.@*Methods@#Twenty-four male C57BL/6J mice (10-14 weeks old) were divided into the terminal experiment group (n=4, for investigating the maximum blood amount that could be sampled at one time), the repeated 0.5 ml blood collection group (n=10, sampling 0.5 ml whole blood each time, once every two days for consecutive 4 weeks), and the repeated 0.75 ml blood collection group (n=10, sampling 0.75 ml whole blood each time, once every two days for consecutive 4 weeks). High-frequency echocardiography was used to display the largest section of the left ventricle, guiding the insulin syringe needle through the thorax into the left ventricle for blood collection. In the repeated 0.5 ml blood collection group, echocardiography was used to detect the cardiac structure and function before blood collection, three minutes after blood collection, and one week after the last (the 14th) blood collection.@*Results@#We successfully performed echocardiography-guided closed-chest intraventricular blood sampling, with an average operating time (88±19)s per mouse, and a maximum blood volume (1.43±0.11)ml per mouse. In the repeated 0.5 ml blood collection group, heart rate, left ventricular ejection fraction, left ventricular fractional shortening, left ventricular end-diastolic dimension and left ventricular posterior wall end-diastolic thickness remained uncganged before the first blood collection and after 4 weeks of repeated blood collection (all P>0.05). No death in the repeated 0.5 ml blood collection group. However, in the 0.75 ml blood collection group, two mice died before the end point.@*Conclusions@#The echocardiography-guided closed-chest intraventricular blood sampling is a safe, minimally invasive, convenient and efficient method, and can be used repeatedly for long-term blood collection in mice.
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Objective@#To investigate and predict the behavioral intention and mode of the protective equipment utilization selection of the workers who used Benzene, the Theory of Planned Behavior (TPB) was applied to establish the behavioral model to enhance the theoretical foundation for long-term intervention.@*Methods@#Questionnaires were used to survey the 707 workers, and all the behaviors of using protective equipment were investigated. Evaluate the relationships between each variable and obtain the influence affects by structural equation model.@*Results@#The investigation showed that 38.47% of the total workers (272 cases) used whole body protection, 13.58% used partially, and 16.69% didn't use any body protection. There were significant difference between the varying degrees in the four dimensions (behavioral attitude, perceived behavior control, subjective norm, and behavioral intention) (P<0.01) . The results of structural equation model revealed that perceived behavior control was the most important influencing factor, subjective norm, positive attitude, negative attitude were the other three respects in sequence. The path co-efficient were 0.600、0.215、0.141 and 0.046 respectively.@*Conclusion@#The study show that the theory of planned behavior can effectively explain the behavioral intention and behavior of protective equipment utilization. Therefore, combining the subjective initiative of individuals with the supervision of enterprises, In order to effectively enhance the protective equipment utilization of benzene workers.
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Objective To study the Bailing capsule combined losartan for UMA and lipid metabolism in patients with early diabetic nephropathy impact analysis.Methods 118 patients with early diabetic nephropathy from October 2015 to May 2016 in our hospital, according to the random lottery was divided into observation group and control group, control group using losartan treatment, observation group on the basis of the combination of Bailing capsule for treatment.Two groups of patients were treated after 3 months, observing two groups of patients with UMA and lipid metabolism related situation, and analyzes the effect of the treatment.Results The UMA ( 125.00 ±44.00 ) mg/24 h and UAER ( 54.64 ±17.31 )μg/min were significantly lower in the observation group than in the control group UMA (216.00 ±46.00) mg/24 h, UAER (67.42 ±21.86) μg/min, 2 group difference was statistically significant (P<0.05).The total cholesterol (TC) of the observation group was (6.15 ±0.75) mmol/L, triglyceride (TG) was (2.34 ±0.48) mmol/L, low density lipoprotein (LDL-C) was (3.55 ±0.73) mmol/L.The levels of TC (6.74 ±0.78) mmol /L, TG (3.01 ± 0.41) mmol/L and LDL-C (4.06 ±0.64) mmol/L, respectively.The levels of TC, TG and LDL-C in the observation group were significantly lower than those in the control group, and high-density lipoprotein (HDL-C) (1.39 ±0.26)mmol/L was significantly higher than that in the control group (1.26 ±0.42) mmol/L, the difference was statistically significant (P<0.05); Two groups of patients after treatment, the observation group total effective rate was 89.7%, significantly higher than that of control group total effective rate 75.0%, two groups are significant difference (P<0.05). Conclusion Bailing capsule combined losartan treatment of early diabetic nephropathy , can effectively reduce the levels of UMA, improve blood lipid in patients with blood sugar levels, which has significant therapeutic effect.
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AIM:We investigated how AT 1-R stimulated by mechanical stresses induces cardiac fibrosis .METHODS:We produced in vivo cardiac pressure overload model in angiotensinogen knockout ( ATG-/-) mice and in vitro mechanically-stretched cell model in cultured neonatal cardiac cells of ATG-/-mice both lack the participation of Ang II .RESULTS: Pressure overload for 4 weeks in ATG-/-mice induced myocardial hypertrophy accompanied by the significant interstitial fibrosis , however , the TGF-β, a key regulatory factor of fibrosis, was not significantly increased in these ATG-/-mice.Meanwhile, the inhibitor for AT1-R significantly inhibited mechani-cal stress-induced cardiac fibrosis in these ATG-/-models whereas inhibition of TGF-βdid not.CONCLUSION:The results showed that mechanical stress-induced fibrotic responses through AT 1-R required the phosphorylation of Smad 2 but not the involvement of TGF-β.
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Objective To establish a Juema minipig model of myocardial infarction, to evaluate the clinical indi?ces in the model pigs, and to explore the relationship between gene expression and metabolic decompensation. Methods 13 male Juema minipigs were randomly divided into control (Sham, n=5), myocardial infarction (MI, n=5) and normal control (for evaluating the recovery condition after surgery, n=3) groups. In the MI group, the ligation was done at the left descending coronary artery around the 1/3 distance to heart apex. Four weeks after the surgery, the cardiac function and serum biochemistry was analyzed. The histological changes and gene expression profiles in the myocardium in the peri?infarct area were exanimated. Results Ultrasonic images showed that the infarction was formed, the ejection fraction and fraction shortening were significantly reduced in the MI group ( ~32% and ~40% less than those of the sham group). Histological examination showed that myocardial fibers at the peri?infarct area were broken, dissolved, and there was con?nective tissue hyperplasia with increased neutrophil and lymphocyte infiltration. Microarray analysis revealed that two myo?cardial remodeling and pathology mediating pathways, three inflammation?related pathways, and 8 metabolic pathways ( in?cluding fatty acid, amino acid, and glucose metabolic pathways) were significantly changed. Conclusions We have suc?cessfully established a Juema minipig model of myocardial infarction. The less branches of the left descending coronary ar?tery allow us to establish a stable model by surgery with comparable characteristics in the clinic indices. The results of this study provides useful reference characteristics of an animal model with characteristic changes in the peri?infarct area.
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Atrial fibrillation ( AF) is an abnormal heart rhythm characterised by rapid and irregular beating.It is caused by multiple factors and can lead to ischemia-associated thrombosis, heart failure and other complex symptoms. Based on the etiology and characteristics of AF, animal models have 3 main categories including electrical, neurohormonal or vessel-related, and structural remodeling models.New technologies such as microRNA knock-down/overexpression or CRISPR-Cas9 gene editing provide tools for constructing animal AF models and directions in the development of AF thera-peutic strategies.Currently these strategies have largely focused on the cellular and molecular therapeutics rather than tradi-tional invasive electrophysiological methods or antiarrhythmic drugs.With the aid of new tools, progress has been greatly made in a broad range of therapeutic research areas including molecular mechanisms, drug targeting and screening.This re-view summarizes the animal models of atrial fibrillation currently used in studies of the molecular and cellular therapeutics and notes their contributions to this research area.
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Aim To observe the change of amyloid, acetylcholine transferase and glial fibrillary acidic protein expression in Macaca Rhesus hippocampal after infused the Aβ_(1-42) and thiorphan and explore the possibility of the establishment of Macaca Rhsus AD model in brain.Method The Rhesus monkeys were anesthetized (im), the skull was exposed by a midline scalp incision, and oriented craniotomy was performed on left side by dental drill.First, neprilysin in cerebral cortex and basal nucleus was consumed by infusion thiorphan. Then cerebral cortex and basal nucleus were slowly infused with fibrilla Aβ_(1-42). Finally, the cannula for thiorphan infusion was implanted into the basal nucleus.Miniosmotic pump (Alzet MODEL 2ML4,) was subcutaneously fixed by bio gel 454 on the calvaria (Loctite Co. Ltd,USA) according to the manufacturer's instructions.After 50 days' survival, animals were deep anesthetized with ketamine and sacrificed. The pathological changes were observed by HE staining and immunostaining in monkey brains.Result Neuronal loss and a proliferation of microglia were detected in hippocampal formation by HE staining.Immuno-staining showed Aβ_(1-42),ChAT and GFAP positive cells density were 0.59±0.05,0.21±0.04 and 0.19±0.04 separately.Compared with control group, the density in experimental groups showed distinct difference in statistic analysis (P<0.01).Conclusion The same pathological change was detected in the thioaphan and Aβ_(1-42) infusion in Macaca Rhesus hippocampal formation as what was found in AD patients.