ABSTRACT
Most of the current experiments are obsolete and verified,the students are not interested in and the experiments are out of touch with the actual work.These are the common problems in the experiment teaching of occupational health and occupational medicine.By taking the students who majored in preventive medicine as the subjects,this study aimed to explore the effects of independent designed experiment teaching mode,which was based on dividing the groups before class,choosing the projects by students themselves,deciding the design of the program via the discussion of teacher and students and doing the experimental reports and sharing the experience.The results showed that,in the premise of the preliminary master of the theory and basic skills of occupational health and occupational medicine,carrying out independent designed experiments in the last three weeks of semester,to a certain extent,could arouse students' interest in learning,cultivate their abilities of independent thinking,practice,problem analysis and solution,and team cooperation.However,restricted by lack of teachers,inadequate equipment and high cost and other factors,this teaching mode is only suitable for small class.
ABSTRACT
In the present study, the single and combined neurotoxic effects of benzo[a]pyrene ([BaP] 0.0, 0.5, and 5.0 mg/kg body weight; intragastric administration) and lead acetate (0.0, 5.4, and 54.0 mg/L; by drinking water) were examined on KunMing mice. In the Morris water maze, results showed that BaP and lead induced synergistic effects on the escape latency and the time spent in the target quadrant but also showed an additive effect on the number of times animal crossing the original platform. Also, BaP and lead induced a synergistic effect on DNA damage in the single-cell gel electrophoresis. However, BaP plus lead showed additive effects on the levels of malondialdehyde, superoxide dismutase, and glutathione. These results suggested that the combination of BaP and lead can lead to a synergistic effect on spatial learning and memory impairments, and the mechanisms of the synergistic effects on behavioral deficits may be due to the oxidative stress injury.
Subject(s)
Benzo(a)pyrene/toxicity , Maze Learning/drug effects , Memory/drug effects , Organometallic Compounds/toxicity , Analysis of Variance , Animals , Apoptosis/drug effects , Comet Assay , DNA Damage , Drug Synergism , Hippocampus/chemistry , Hippocampus/drug effects , Hippocampus/metabolism , Hippocampus/pathology , Male , Malondialdehyde/metabolism , Mice , Oxidative Stress/drug effectsABSTRACT
Polybrominated diphenyl ethers (PBDEs), a class of widely used flame retardants, are extensively diffused in the environment. Of particular concern are the reported highly sensitivity of PBDEs in children or developmental animals, however, almost no information is available on their potential effects on adults and the mechanisms are still unknown. In the present study, we investigated the neurotoxic effects of sub-chronic PBDE-47 exposure on adult male Sprague-Dawley rats. Thus, PBDE-47, 0.1, 0.5 and 1 mg/kg per day was administered to rats by gavage for 30 days. The learning and memory function was tested by Morris water maze. Further, in order to explore the potential mechanism, the expression of NMDA-receptors was evaluated by using both immunohistochemistry (IHC) and RT-PCR. Our results showed that sub-chronic exposure to PBDE-47 produced learning and memory deficits in male adult rats. Also, significant decrease in the CA1, CA3 and dentate gyrus areas of hippocampus affected by all three doses of PBDE-47 on the expression of NR(1), NR(2)B and Glu were found by IHC. In addition, the evaluation of expression of the NR(1), NR(2)B and NR(2)C showed statistically significant decrease in mRNA expression in rats exposed to PBDE-47. These findings showed that sub-chronic exposure to PBDE-47 could also induce behavioral alterations and the neurotoxic effects might due to the down-regulation expression of NMDA receptors. Our data indicated that the possibility of exposure of adults to PBDE-47 warranted further studies to characterize their potential neurotoxicity.
Subject(s)
Environmental Pollutants/toxicity , Flame Retardants/toxicity , Halogenated Diphenyl Ethers/toxicity , Maze Learning/drug effects , Memory Disorders/chemically induced , Animals , Hippocampus/drug effects , Hippocampus/metabolism , Male , Maze Learning/physiology , Memory Disorders/metabolism , RNA, Messenger/metabolism , Rats , Rats, Sprague-Dawley , Receptors, Glutamate/metabolism , Receptors, N-Methyl-D-Aspartate/genetics , Receptors, N-Methyl-D-Aspartate/metabolismABSTRACT
Spatial learning and memory (LM) is a property of central importance in the nervous system, yet many of the molecular mechanisms for benzo(a)pyrene[B(a)P]-induced LM deficits remain enshrouded in mystery. In this study, influence of exposure to B(a)P on LM deficits in adult male Sprague-Dawley rats was evaluated by Morris water maze. Then morphological changes in the ultramicrostructure of hippocampal neurons were observed by transmission electron microscopy. Furthermore, to better understand the molecular changes that occur in B(a)P induced LM deficits, antibody-based protein microarrays was used to analyze protein expression changes in rats submitted to sub-chronic oral gavage of B(a)P (2 mg/kg for 90 days). Results suggested that rats in the B(a)P-treated groups have significantly impaired Morris water maze performance when compared to controls. Meanwhile, the B(a)P-induced neuronal damage was also found in the hippocampus under transmission electron microscopy. Our results demonstrate that LM deficits associated protein expression signatures could be identified from tissue proteomes, as well as potential biomarkers such as retinoic acid receptor b (RARb), synaptotagmin iosfomrs 1 (Syt1) and Brain-derived neurotrophic factor (BDNF), previously not found. This study, therefore, identifies, for the first time, multiple novel proteins that are dysregulated by B(a)P, which both enhance our understanding of B(a)P induced LM deficits and represent targets of novel therapeutics.
Subject(s)
Benzo(a)pyrene/toxicity , Carcinogens/toxicity , Learning Disabilities/chemically induced , Maze Learning/drug effects , Memory/drug effects , Neuropeptides/metabolism , Animals , Hippocampus/drug effects , Hippocampus/metabolism , Hippocampus/pathology , Learning Disabilities/metabolism , Male , Maze Learning/physiology , Memory/physiology , Neurons/drug effects , Neurons/metabolism , Neurons/ultrastructure , Rats , Rats, Sprague-Dawley , Tissue Array AnalysisABSTRACT
OBJECTIVE: Noise has always been an important environmental public health issue for mankind. Although reports exist on hippocampal-dependent spatial learning and memory (LM) impairment due to noise, there are only a few studies that have examined the effects of recovery from noise stress on LM impairments. Therefore, the present study investigated the effects of recovery from chronic noise exposure on LM deficits. MATERIALS AND METHODS: In this study, the detrimental effects of noise stress on young male rats in the Morris water maze (MWM) were investigated at 1, 10, 20, 30, and 40 days after the discontinuation of chronic noise exposure of 80 dB or 100 dB for 4 h per day, for 30 days. The levels of monoamine neurotransmitters in the hippocampus were also evaluated by HPLC-EC at the end of each behavioral test. RESULTS: Statistical analysis revealed that rats in the noise-treated groups failed to reach the same level of performance as the controls in the MWM. Further, the levels of dopamine (DA), norepinephrine (NE) and 5-hydroxytryptamine (5-HT) were significantly decreased in the hippocampus after noise exposure. However, the reduction in monoamine levels and impaired water maze performance recovered over time, so that by 30th day after cessation of noise exposure the 80 dB group showed no performance difference from the controls, and by 40th day, the 100 dB group also showed no performance difference from the control. CONCLUSION: Our findings suggest that noise impaired LM in young male rats and reduced monoamine neurotransmitters in the hippocampus. However, the noise-induced water maze deficits recovered over time, and the concurrent restoration of hippocampal monoamine neurotransmitter levels suggest that they are involved in LM impairments.
Subject(s)
Maze Learning , Memory Disorders/etiology , Noise/adverse effects , Animals , Disease Models, Animal , Glycine Plasma Membrane Transport Proteins , Learning , Male , Maze Learning/physiology , Memory Disorders/metabolism , Norepinephrine/analysis , Norepinephrine/metabolism , Rats , Recovery of Function , Serotonin/analysisABSTRACT
A single factor duplicate test was designed to investigate whether bovine recombinded resistin impacts the expression of pyruvate carboxylase (PC) mRNA and the activity of PC in vitro culture bovine hepatocyte.Bovine recombinded resistin was added to the media with 0,25,50,100,200 and 400 ng/L.Abundance of PC mRNA in bovine hepatocyte,which was cultured with bovine recombinded resistin for 12 hours,was determined by real-time fluorescence quantitative RT-PCR,and activity of PC was determined by colourimetry.The results showed that bovine recombinded resistin could downregulate the expression of PC mRNA and the activity of PC in vitro culture bovine hepatocyte.
