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兴趣是最好的老师,是学生学习的法宝。兴趣是提高课堂教学质量的有效保障。因此,教师要熟练地掌握教材,充分准备好每一节课,运用灵活多样的教学方法,激发学生浓厚的学习兴趣。怎样提高学生的学习兴趣呢?下面谈谈我的几点建议。
一、注重新课导入
新课的导入是激发学生听课的积极性、提高授课效率的关键环节。风趣幽默,激情澎湃且紧扣主题的导入,会吸引学生的注意力,调动学生的好奇心,增强学生的求知欲,能进入最佳学习状态,提高听课质量。例如在教授“地球仪”这一课时,先给学生讲一个小故事:有一位县城中学的地理老师去给乡下中学的同学们讲课,老师指着讲桌上歪着身子的地球仪问学生:“是谁弄坏的?”大家都说不是自己。这时校长正好从门口经过,赶忙进来替那位同学解释到:“这不怪学生,是学校经费紧张,这些地球仪是从地摊上买来的便宜货。”那位老师听罢便给同学们解释:“老师只是跟你们开个玩笑而已,这个地球仪并没有坏。其实地球仪本身就是围绕着地轴斜着身子在转动”。通过这样的故事导入,激发了学生学习的兴趣,使学生产生了求知欲望。
二、课堂联系实地
初中生初步具备了直观感受外界事物的能力。在教学过程中,我们应尽量拓展和使用日常生活中潜在的兴趣材料。在讲“地球的运动”时,通过身边的事例:太阳的东升西落,一年中有春、夏、秋、冬,四季的变化规律,让学生大胆的说出自己的理解。通过这种课堂与生活相联系的模式,让学生自己总结归纳一些地理知识概念,使学生明白自然界的某些现象其实就在我们生活的周围,用生活中的现实教材加以辅助,培养他们观察、分析问题、解决问题的能力,逐渐提高他们的学习兴趣。
三、做到寓教于乐
作为地理老师。应该积累更多的知识,在平时的授课过程中把生动有趣的故事运用到课堂中,会使枯燥乏味的课堂变化得妙趣横生,很受欢迎。如讲到“季风气候”一节时,“季风”本身就是气候方面的一个难点,学生难于理解,在授课中我建议引用古典名著《三国演义》中诸葛亮“巧借东风,火烧曹营”的故事引出季风这一难点。
四、融入多元模式
地理课堂不仅可以让学生树立空间概念,同时我觉得还可以锻炼学生的审美观念。因此,把历史背景巧用于课堂中,会创造出一种诗情画意般的教学意境,能起到出“奇”制胜的作用。如在教学“祖国的神圣领土――台湾”一课时,先让学生观看民族英雄郑成功的影像资料,使他们从一开始就明白台湾自古以来就是祖国不可分割的神圣领土,由于种种原因使其与大陆不能团聚,但两岸人民都在努力,台湾最终还是会回到祖国母亲的怀抱。这样就能唤起学生对台湾的无限向往,对祖国的无限热爱。既提高了学生兴趣,又增强了学生听课的积极性,还培养了学生的爱国情感,一举多得。
五、重视探究解惑
古人云:“学贵有疑,小疑则小进,大疑则大进。疑者,觉悟之机也,一番觉悟,一番长进。”其实各种授课方式贵在巧设疑问,激发兴趣,调动学生思维。作为教师,在教学中还要学会善于设问,只有这样,才能激起学生的好奇心,达到培养兴趣的目的。
六、拓展想象空间
中图分类号:G633.5文献标识码:B文章编号:1672-1578(2015)08-0252-01
我们在河北省十二五规划课题《理答行为与初中地理课堂教学有效性的实践研究》研究前期,对理答行为进行了概念界定:理答行为是教师对学生学习行为的反应,即教师根据学生所思、所答、所学是否正确、充分、恰当的程度,给予指导、点拨、引领、评价,帮助学生调整、控制后续学习行为。理答既是一种教学行为,也是一种教学环境。
理答行为,直接影响着地理课堂中学生学习的有效和高效,地理教师理答行为的有效、科学、艺术对学生发展有促进作用。我们总结出地理教师课堂理答时应注意以下事项。
1.增强理答意识,提升学生学习的有效性
我们课题组在研究过程中多次感受到:地理课堂中,教师理答意识的缺失,导致我们的地理课堂丢失很多精彩,课堂有效性受到影响。
案例1:一地理教师在讲授人教版八年级下册第八章第一节《西北地区的自然特征与农业》时,谈到"西北地区怎么保护水资源?"师说:"坎儿井、万里长城、京杭运河被称为我国三大奇迹,你对坎儿井,有何感想?"有些学生直截了当地说:"我不知道坎儿井是什么,没什么感想。"师说:"大家看教材P77图8-12,你们能看懂这些坑吗?"生答:"看不懂。"
案例2:一地理教师出差20天,回来上课,学生很兴奋,学习主题"我国铁路干线的分布"。她是这样导入的:"老师出差去重庆,你帮老师选择一下恰当的交通运输方式:1.最省钱;2.最快到达。"
"老师,你走着去,最省钱";"老师,骑马去、不累还省钱";"坐120去…";"做梦去…";"坐火车去…";"坐轮船去…";"坐飞机去…"
十四五岁的学生无拘无束,思维敏捷,活泼调皮,这样很正规的导入,也能让他们像瞬时像决堤的洪水一泻千里。面对学生们的不靠谱,她是很严肃地这样进行理答的:"20天没见,各位思考问题的速度与日俱增。
该教师面对学生这种状况,积极理答,短短几句话,就把学生的思维引导主题学习上,学习有效性得到提升。
2.重视理答预设,提高课堂教学实效性
我们课题组在研究过程中发现:优秀地理教师在教学设计上独具匠心,把课堂中可能的现象尽可能全面考虑,把理答的预设做的尽可能完善。他们发展性理答的多样性、激励性理答的激励性、诊断性理答的引导性是典型的智慧理答特征。他们游刃有余地驾驭课堂,都曾经历过最初的充分准备过程。
3.理答突出教学风格,提升地理课堂魅力
预设,仅仅对我们的地理课堂理答行为提供了保障,奠定了基础,让地理教师在执教过程中做到胸有成竹,但动态课堂并非所有的一切都能被我们预设到,孩子丰富多彩的回答,我们不可能面面俱到、考虑周全,地理课堂的精彩就在于无法预设的理答行为中,这就需要地理教师在动态课堂中不断磨练自己的理答水平。
4.理答关注学生发展,提升学生学习智慧
有效、科学、艺术的理答最大受益者是学生,因此关注学生的发展在理答行为显得尤为重要。地理课堂上老师精彩有效的激励性理答对学生学习和心理的影响是举足轻重的,既能充分调动学生求知的积极性,又能给学生指明思考问题的方向,而且能让学生在解决问题的过程中,起到"四两拨千斤"之功效,往往能使原本陷入僵局的课堂气氛,一下子活跃起来。
案例1:人教版八年级上册《2-1地形和地势》主题学习。
一地理教师的总结让我记忆尤深:"这节课,我们学习的知识点是中国地势特征――三阶梯。其实,地理的学习也分三级阶梯。
第一级,就是这幅图的填写。只要有眼睛,认识字,就能够从地图上找准这些地理名称,并准确填在图上,不需要怎么动脑。如果你仅停留在这一台阶,充其量你就是一个知识的容器。
第二级,就是根据我们所描画的这张图,提炼并分析地理信息,就像板书上咱们一起画的这个阶梯示意图,和咱们总结的地势特征这句话,这需要稍稍动一下脑筋。
第三级,就是右边箭头所指的这部分,今天所学的"地势和其它地理要素间的关系",是本节课最高层次的学习,它需要我们开动脑筋,调动所有的知识储备,把今天所学和以往所学联系起来,分析他们是如何相互影响的。我们不要仅限于做知识的容器,应该立志做榨汁机,把不同的蔬果调和成好喝且营养丰富的果汁,这样的学习才会让你变得聪明和智慧。老师希望你们不仅有学识,更希望你们在地理课堂上变得越来越聪明。所以,希望我们在以后的地理课堂中,按照今天的学习模式锻炼自己的思维,勤思考,多提问,让自己变得越来越聪明。"
随后,该老师还进一步归纳出了三段式学习方式:
(1)看图,明晰地图上的地理信息――第一阶梯学习:即地图上有什么?在哪?
在地理课堂教学过程中,经常出现的不当行为,就是要求学生死记硬背地理知识点,这是非常错误的。我们知道一些地理信息是需要学生死记硬背的,但把地理学习理解成死记硬背知识点就极为错误了。原因是教师对地理课程的性质把握不准,没有树立地理课程理念,造成教学目标不合理,教法单一,片面抓识记这一层面的教学,其结果是学生只背得几个知识点,而理解、运用层面的能力没有得到训练,效率低下。
针对这样的问题:(1)教师要吃透课标和教材,真正认识地理课程是素质教育这个系统中重要的一环,地理课堂教学应引导学生同时进行识记、理解、运用三个层面的训练,这样就从思想根源上矫正了片面要求学生死记硬背的不当行为;(2)教师要不断提高专业素养,精心设计教学过程,课堂上突出读图分析的引导,培养学生使用地图的习惯,并掌握使用地图的方法;(3)在教学评价中对学生识记、理解、应用的情况全面考查,尤其考查读图、用图能力,摒弃死记硬背。
二、重传授课本知识轻实践活动,不利于学生能力发展
有部分地理教师在课堂上一味传授课本上的知识,也善于总结知识,将知识系统归纳得很到位,并通过书面练习来促使学生巩固知识,这样的教师很受欢迎,因为学生可以在考试中拿到高分,但往往忽视开展地理实践活动。地理课程注重培养学生从地理视角思考问题,而不仅仅是记住书本上的地理知识去应付中考。要想矫正这样的课堂教学行为,就要开展好地理实践活动。如指导学生动手制作、进行地理观测活动等,确保学生有合理的课堂实践时间,培养初中学生观察能力、综合思维能力、实践能力。
Mercury(Hg) is a hazardous heavy metal, which could be released into the environment from both natural and anthropogenic sources. Natural sources of Hg include volcanic emissions, volatilization from the ocean, and degassing from soil. Use of Hg in industrial such as the manufacture of plastic, chlorine, caustic soda, caustic potash and antifouling paint, is the major anthropogenic sources. Use of Hg in agriculture such as fossil fuel burning, base metal smelting, waste incinerators and Hg based fungicides are other important input sources of Hg in the environments[1]. In addition, there is a high potential for Hg bioaccumulation and biomagnification in different organisms. The levels of Hg in some commercial fish in New Jersey were detected in the range known to cause some sublethal effects in sensitive predatory birds and mammals[2]. High levels of Hg content were also found in commercial pelagic fish in the Western Indian Ocean, and large fish can naturally bioaccumulate Hg[1]. Especially, in the summer of 2 000, Hg spills were discovered in the basements of some Chicagoarea homes after removal of gas regulators by gas company contractors[3]. The risk of residential Hg contamination after gas regulator removal ranged from 0.9/1 000 to 4.3/1 000 homes[3]. So far, Hg has been considered as one of the most serious environmental contamination threats to human, fish and wildlife of the global.
Mice, rodents, fish, birds and some other mammals have ever been used as models to evaluate the Hg toxicity and related regulation mechanisms. Elemental Hg is a silvery metal that is liquid at room temperature. Human absorption of elemental Hg occurs primarily through inhalation of Hg vapor[3]. The primary targets of acute exposure to Hg are liver, kidneys and central nervous system in fish, birds and mammals[4-5]. Inhaled Hg vapor results in accumulation with highest concentrations in the cerebellum and brainstem nuclei of rats and mice[6]. Hg can cause toxic effects at concentrations even below 1 ppb in water and the effects include loss of appetite, brain lesions, cataracts, abnormal motor coordination and abnormal behavioral changes[4-5,7]. Aspects affected by Hg exposure also contain the reproduction, growth, metabolism, blood chemistry, immunity, and oxygen exchange[8-11]. Several theories about the mechanism of Hg toxicity have already been raised and these theories suggest that the Hg exposure can cause multibiological toxicities by affecting specific signaling pathways and lipid peroxidation[12-13]. However, for the possible limit of the experimental organisms of mice, fish, birds and other mammals, whether the multibiological toxicities caused by Hg exposure can be transferred from exposed animals to their progeny remains still unclear.
Caenorhabditis elegans, a freeliving soil nematode, has been found favor as a biomarker organism, because it is one of the bestcharacterized animals at the genetic, physiological, molecular, and developmental levels[14]. C. elegans has the properties of short life cycle, small size, ease of cultivation, a simple cell lineage that has been completed characterized, and behavior easily monitored under the microscope. Moreover, its great potential for forward and reverse genetic analysis make it very powerful for deeply elucidating the mechanisms of metal toxicity. By virtue of these properties, several toxicity tests using C. elegans have been developed for ecological risk assessment in soil[15-16] and water[17-19]. Moreover, transgenic hsp16GFPlacZ and hsp16GFP nematodes have been constructed for the study of environmental monitoring and toxicology[20-25]. In addition, a standardized method for conducting laboratory soil toxicity tests using C. elegans was published in the America Society for Testing and Materials(ASTM) Guide E217201 in 2002[26].
In the present study, we selected the C. elegans organism to examine whether the multibiological toxicities induced by Hg exposure can be transferred from exposed animals to their progeny. Our results suggest that most of these multibiological toxicities induced by Hg exposure can be considered to be transferable from parental generations to their progeny, and some specific defects in progeny appeared even more severe than in their parental generations.
1 Materials and methods
1.1 Chemicals
The Hg concentrations used in this report were selected as previously described[20,27]. Three concentrations of HgCl2 solution were used in the current work, and they were 2.5 μmol·L-1, 75 μmol·L-1 and 200 μmol·L-1, respectively. All the chemicals were obtained from SigmaAldrich(St. Louis, MO, USA).
1.2 Strains
All nematodes used were wildtype N2, originally obtained from the Caenorhabditis Genetics Center(CGC). They were maintained on nematode growth medium(NGM) plates seeded with Escherichia coli OP50 at 20 ℃ as described[28]. Gravid nematodes were washed off the plates into centrifuge tubes and were lysed with a bleaching mixture(0.45 mol·L-1 NaOH, 2% HOCl). Age synchronous populations of N2(L4larvae stage) were obtained by the collection as described[29]. The L4larvae stage nematodes were washed with doubledistilled water twice, followed by washing with K medium once(50 mmol·L-1 NaCl, 30 mmol·L-1 KCl, 10 mmol·L-1 NaOAc, pH 5.5). Exposures were performed in 12well sterile tissue culture plates. All exposures were 48h, and were carried out in 20 ℃ incubator in the absence of food. To evaluate the Hg toxic in progeny, eggs were obtained from nematodes subjecting to the Hg exposure with the bleaching mixture, and then transferred to a normal NGM plates without addition of Hg solution. Endpoints of lifespan, body size, body bend, head thrash, and chemotaxis plasticity were used for the acute toxicity testing in C. elegans.
1.3 Lifespan and body size
The methods were performed as previously described[30-32]. For life span assay, the exposed and progeny animals were picked onto the assay plates and the time was recorded as t=0. About twenty animals were placed onto a single plate and adult animals were transferred every 2 days to fresh plates during the brood period. The numbers of survivors were scored every day. Animals that failed to respond to repeated touch stimulation were considered as dead. Life span graphs are representative of at least three trials. Body size was determined by measuring the flat surface area of nematodes using the ImagePro Express software. For each test, at least 15 animals were picked for assay.
1.4 Head thrash frequency
The thrashes were assayed as previously described[33-35]. To assay the head thrash frequency, nematodes were washed with the doubledistilled water, followed by washing with K medium. Every animal was transferred into a microtiter well containing 60 μl of K medium on the top of agar. After a 1 min recovery period, the head thrashes were counted for 1 min. A thrash was defined as a change in the direction of bending at the mid body. Fifteen nematodes were examined per treatment.
1.5 Body bend frequency
The method was performed as previously described[33-35]. To assay the body bend frequency, nematodes were picked onto a second plate and scored for the number of body bends in an interval of 20 s. A body bend was counted as a change in the direction of the part of the animals corresponding to the posterior bulb of the pharynx along the y axis, assuming that the nematodes were traveling along the x axis. Fifteen nematodes were examined per treatment.
1.6 Chemotaxis assay and conditioning procedure
Chemotaxis assays and conditioning procedure were performed as previously described[22,36]. Approximately 100 nematodes were used for each trial. An agar plug excised from the plate with additional 100 mmol·L-1 NaCl was placed on the surface of assay plate containing 5 mmol·L-1 potassium phosphate, pH 6.0, 1 mmol·L-1 CaCl2, 1 mmol·L-1 MgSO4 and 20 g·L-1 agar for at least 14 h. Shortly before analysis, the plug was removed and 1 μl 0.5 mol·L-1 NaN3 was spotted at the centre of plug to anaesthetize the nematodes. NaN3 was also spotted 4 cm away from the centre of the NaCl gradient as a control. The chemotaxis index CI was calculated as CI=(the number within NaCl gradientthe number within control) / the total number of nematodes on the plate.
To analyze the learning, the treated nematodes(young adults) were washed three times with washing buffer containing 5 mmol·L-1 potassium phosphate, pH 6.0, 1 mmol·L-1 CaCl2, 1 mmol·L-1 MgSO4 and 0.5 g·L-1 gelatin. Nematodes were starved for 3 h at NaClE. coil plates(NaClfree and E. colifree plates) or+NaClE. coil plates. And then, they were collected with washing buffer and placed equidistant(about 3.5 cm) from those two spots mentioned above on the assay plate to let them move freely for 45 min at 20 ℃. The nematodes within 1.5 cm of these two spots were counted.
1.7 Statistical analysis
All data in this article were expressed as means ± S.D. Graphs were generated using Microsoft Excel(Microsoft Corp., Redmond, WA). An overall ANOVA was used for comparison between control and the metal treated groups, followed by pairwise comparison tests. The probability levels of 0.05 and 0.01 were considered statistically significant.
2 Results
2.1 Lifespan defects in Hg exposed nematodes and their progeny Lifespan is often used as a main parameter to evaluate the toxicity of a specific metal or compound in nematodes[19,22,31]. Because C. elegans has a very short life cycle, it is more convenient to investigate the aging and to elucidate the mechanism of animals lifespan[30]. In other organisms, Hg was found to be able to accelerate the aging process possibly by affecting the neurotoxicity and oxidative injury[13]. In C. elegans, as shown in Fig 1, high concentrations(75 μmol·L-1 and 200 μmol·L-1) of Hg exposure caused more severe lifespan defects compared to low concentration(2.5 μmol·L-1) of Hg exposure and control(0 μmol·L-1). When nematodes were exposed to 75 μmol·L-1 and 200 μmol·L-1 concentrations of Hg, their maximum lifespans were reduced by nearly 4 days compared to control. The mean lifespans of nematodes exposed to 200 μmol·L-1 Hg was nearly half of those in control nematodes.
A. Lifespans of nematodes exposed to 2.5 μmol·L-1 Hg. B. Lifespans of nematodes exposed to 75 μmol·L-1 Hg. C. Lifespans of nematodes exposed to 200 μmol·L-1 Hg. D. Lifespans of progeny from nematodes exposed to 2.5 μmol·L-1 Hg. E. Lifespans of progeny from nematodes exposed to 75 μmol·L-1 Hg. F. Lifespans of progeny from nematodes exposed to 200 μmol·L-1 Hg.G. Comparison of the mean lifespan for nematodes exposed to 2.5 μmol·L-1, 75 μmol·L-1 and 200 μmol·L-1 Hg, respectively.H. Comparison of the mean lifespan for progeny from nematodes exposed to 2.5 μmol·L-1, 75 μmol·L-1 and 200 μmol·L-1 Hg, respectively. Bars represent mean ± S.D. a. P
Fig 1 Lifespans of nematodes exposed to different concentrations of Hg and their progeny To investigate whether the Hg toxicity on lifespan could be transferred from exposed nematodes to their progeny, we analyzed the changes of lifespan in progeny of nematodes exposed to Hg. Surprisingly, the toxicity on lifespan from Hg exposure could not be obviously recovered in progeny nematodes. Severe defects could still be observed for both the maximum lifespan and the mean lifespan in progeny nematodes. Therefore, the toxicity on lifespan from Hg exposure can be transferred from exposed nematodes to their progeny, and Hg exposure can exert severely adverse effects on the lifespan of progeny nematodes.
2.2 Developmental defects in Hg exposed nematodes and their progeny We next examined the effects of Hg exposure on nematode development by observing the body size and morphology of animals. As shown in Fig 2, the body sizes of nematodes were significantly(P
0 μmol·L-12.5 μmol·L-175 μmol·L-1200 μmol·L-1Hg exposedProgeny
A. Morphological comparison of nematodes exposed to different concentrations of Hg and their progeny. All images are representative of threeday post hatch nematodes.B. Comparison of body sizes of nematodes exposed to different concentrations of Hg. C. Comparison of body size of progeny from nematodes exposed to different concentrations of Hg. Bars represent mean ± S.D. a. P
Fig 2 Body sizes of nematodes exposed to different concentrations of Hg and their progeny
In addition, high concentrations of Hg exposure usually caused the appearance of very slim nematodes, and more nematodes with this phenotype were found in progeny population. Thus, more severe development defects can be formed in progeny of nematodes exposed to Hg.
2.3 Locomotion behavior defects in Hg exposed nematodes and their progeny Hg exposure can not only influence the lifespan and the development, it may also affect the development and function of nervous system[34]. To test the influences of Hg exposure on locomotion behaviors, the body bend and the head thrash were assayed. As shown in Fig 3, both the body bends and the head thrashes in nematodes were dramatically impaired even exposed to a very low concentration of 2.5 μmol·L-1 Hg. More severe body bend defects were observed when nematodes were exposed to high concentrations(75 μmol·L-1 and 200 μmol·L-1) of Hg, whereas no distinct differences were found for the head thrash defects in nematodes exposed to 2.5 μmol·L-1 of Hg from those in nematodes exposed to 75 μmol·L-1 and 200 μmol·L-1 of Hg. Investigation on their progeny indicates that the defects of body bends could be largely or completely recovered. The defects of head thrashes could be largely recovered in nematodes exposed to 2.5 μmol·L-1 of Hg, and the head thrash frequencies in progeny of nematodes exposed to 75 μmol·L-1 and 200 μmol·L-1 of Hg could be recovered approximately 21% and 14%, respectively.
A. Body bend frequencies of nematodes exposed to Hg. B. Body bend frequencies in progeny of nematodes exposed to Hg.C. Head thrash frequencies of nematodes exposed to Hg.D. Head thrash frequencies in progeny of nematodes exposed to Hg. Bars represent mean ± S.D. a. P
Fig 3 Locomotion behaviors of nematodes exposed to different concentrations of Hg and their progeny
2.4 Chemotaxis plasticity defects in Hg exposed nematodes and their progeny The chemotaxis plasticity is one of the simple forms for behavioral plasticity, which might be able to reflect a form of associative learning[36]. Lastly, we examined the possible toxic effects of Hg exposure on nematodes chemotaxis plasticity. In this research system, the conditioning requires both the presence of NaCl and the absence of a bacterial food source, because starvation on culture medium containing the NaCl can make the chemotaxis of animals towards to NaCl fall dramatically[36]. As shown in Fig 4, nematodes exposed to 75 μmol·L-1 and 200 μmol·L-1 concentrations of Hg displayed severe chemotaxis plasticity defects(P
Taken together, our data suggest that Hg exposure can result in the transferable toxicities or defects for both the locomotion behaviors and the behavioral plasticity from exposed nematodes to their progeny in C. elegans.
A. Chemotaxis performance of nematodes exposed to Hg. B. Chemotaxis performance in progeny of nematodes exposed to Hg. About 100 nematodes were put on each plate. CI=(the number within NaCl gradientthe number within control) / the total number of nematodes in plate. Bars represent mean ± S.D. a. P
Fig 4 Chemotaxis plasticity of nematodes exposed to different concentrations of Hg and their progeny
3 Discussion
Hg exposure in the environment is one of the most increasing health concerns so far. Its ability to form monomethyl mercury through microbe biotransformation leads to accumulation in the food chains. In C. elegans, early in 1982, Popham and Webster ever analyzed the ultrastructural changes of animals exposed to Hg[37]. The stress response, mortality, reproduction, and structures and functions of sensory neurons were also examined previously in Hg exposed nematodes[20,23,38-40]. However, the systematical multibiological toxicities have not been investigated yet. In this report, endpoints of lifespan, body size, body bend, head thrash, and chemotaxis plasticity were used for the acute toxicity testing to examine the multibiological toxicities from Hg exposure. Our results indicate that the Hg exposure could cause multibiological defects with a concentrationdependent manner in C. elegans, which are largely consistent with the conclusions drawn from other organisms[1-13].
Moreover, among these multibiological toxicities, we found that the developmental defects are very specific for the Hg toxicity. Hg exposure specially caused the appearance of slim animals at high concentrations. Metallothionein gene expression in the larvae of C. elegans has been raised as a potential biomarker for Hg toxicity[41]. However, the metallothionein gene expression can also indicate the toxicity from cadmium exposure. Therefore, the morphological defects will be valuable to be used as a key monitor to evaluate the specific Hg toxicity from environments. Especially, a combination of this phenotype with the transgenic reporter for metallothionein gene would be more valuable for the assessment of the Hg toxicity.
According to the results and analysis in this project, we can summarize the defects caused by Hg exposure into four groups based on the transferable properties from exposed nematodes to their progeny. First, the defects caused by Hg exposure could be largely recovered in progeny, such as the locomotion behaviors in progeny of nematodes exposed to low concentration of Hg. Second, the defects caused by Hg exposure could be only partially recovered in progeny, such as the chemotaxis plasticity. Third, no rescue phenomena could be observed for the defects caused by Hg toxicity, such as the body sizes in progeny of nematodes exposed to low concentration of Hg. Fourth, the defects caused by Hg toxicity became more severe in progeny than in their parents, such as the body sizes in progeny of nematodes exposed to high concentrations of Hg. Thus, our data suggest that the multibiological defects of phenotypes and behaviors caused by Hg exposure could largely be considered as transferable in C. elegans.
However, the transferable properties of Hg exposure could not be considered as a kind of heredity in genetics, since some of the defects caused by Hg exposure could still be partially recovered in progeny nematodes. Therefore, we suppose that gain of the transferable properties for nematodes exposed to Hg might be largely due to the deposition of Hg toxicity in their eggs. Organic and inorganic Hg has been found to be able to be all transferred to the fetal rat via placenta and milk[42-43]. Residual Hg levels in egg yolk were also found to greatly surpass the level found in the egg white[44]. But at the same time, we also noticed that some of the defects in progeny nematodes appeared even more severe phenotypes than in their parents, which is still an interesting question needed to be deeply elucidated.
In conclusion, our results showed that the Hg exposure can result in multitoxicity, and most of these multibiological defects can be transferred to progeny from Hg exposed nematodes.
Acknowledgements Strain used in this work was provided by the Caenorhabdits Genetics Center(funded by the NIH, National Center for Research Resource). This work was supported by the grants from the National Natural Science Foundation of China(No. 30870810) and the Program for New Century Excellent Talents in University.
参考文献
[1] KOJADINOVIC J, POTIER M, CORRE M L, et al. Mercury content in commercial pelagic fish and its risk assessment in the Western Indian Ocean[J]. Sci Total Environ, 2006,366:688700.
[2] BURGER J, GOCHFEILD M. Heavy metals in commercial fish in New Jersey[J]. Environ Res, 2005,99:403412.
[3] HRYHORCZUK D, PERSKY V, PIORKOWSKI J, et al. Residntial mercury spills from gas regulators[J]. Environ Health Persp, 2006,114:848852.
[4] SUNDBERG J, JONSSON S, KARLSSON M O, et al. Lactational exposure and neonatal kinetics of methylmercury and inorganic mercury in mice[J]. Toxicol Appl Pharm, 1999,154:160169.
[5] BECKVAR N, DILLON T M, READ L B. Approaches for linking wholebody fish tissue residues of mercury or DDT to biological effects thresholds[J]. Environ Toxicol Chem, 2005,24:20942105.
[6] CASSANO C B, VIOLA P L, GHETTI B, et al. The distribution of inhaled mercury(Hg203) in the brain of rats and mice[J]. J Neuropath Exp Neurol, 1969,28:308320.
[7] ZANOLI P, CANMAZZA G, BARALDI M. Prenatal exposure to methyl mercury in rats:focus on changes in kynurenine pathway[J]. Brain Res Bull, 2001,55:235238.
[8] BULAT P, DUJIC L, POTKONJAK B. Activity of glutathlone peroxidase and superoxide dismutase in workers occupationally exposed to mercury[J]. Int Arch Occup Environ Health, 1998,71(Suppl): s3739.
[9] BULLEIT R F, CUI H. Methylmercury antagonizes the survivalpromoting activity of insulinlike growth factor on developing cerebellar granule neurons[J]. Toxicol Appl Pharmacol, 1998,153:161168.
[10] HULTMAN P, NIELSEN J B. The effect of dose, gender, and nonH2 genes in murine mercuryinduced autoimmunity[J]. J Autoimmun, 2001,17:2737.
[11] GOULET E D, MIRAUL T M E. Neurobehavioral changes in mice chronically exposed to methylmercury during fetal and early postnatal development[J]. Neurotoxicol Teratol, 2003,25:335347.
[12] BASU N, STAMLER C J, LOUA K M, et al. An interspecies comparison of mercury inhibition on muscarinic acetylcholine receptor binding in the cerebral cortex and cerebellum[J]. Toxicol Appl Pharmacol, 2005,205:7176.
[13] SATO M, KONDOH M. Recent studies on metallothionein: Protection against toxicity of heavy metals and oxygenfree radicals[J]. Tohoku J Exp Med, 2002,196:922.
[14] RIDDLE D L, BLUMENTHAL T, MEYER B J, et al. C. ELEGANS Ⅱ [M]. New York: Cold Spring Harbor Laboratory Press, Plainview, 1997.
[15] PEREDNEY C L, WILLIAMS P L. Utility of Caenorhabditis elegans for assessing heavy metal contamination in artificial soil[J]. Arch Environ Contam Toxicol, 2000,39:113118.
[16] GRAVES A L, BOYD W A, WILLIAMS P L. Using transgenic Caenorhabditis elegans in soil toxicity testing[J]. Arch Environ Contam Toxicol, 2005,48:490494.
[17] TRAUNSPURGER W, HAITZER M, HSS S, et al. Ecotoxicological assessment of aquatic sediments with Caenorhabditis elegans(nematode)—a method testing liquid medium and wholesediment samples[J]. Environ Toxicol Chem, 1997,16:245250.
[18] MUTWAKIL M H A Z, READER J P, HOLDICH D M, et al. Use of stressinducible transgenic nematodes as biomarkers of heavy metal pollution in water samples from an English river system[J]. Arch Environ Contam Toxicol, 1997,32:146153.
[19] WANG X Y, SHEN L L, YU H X, et al. Toxicity evaluation in a paper recycling mill effluent by coupling bioindicator of aging with the toxicity identification evaluation method in nematode Caenorhabditis elegans[J]. J Environ Sci, 2008,20:13731380.
[20] CHU K W, CHOW K L. Synergistic toxicity of multiple heavy metals is revealed by a biological assay using a nematode and its transgenic derivative[J]. Aquat Toxicol, 2002,61:5364.
[21] DAVID H E, DAWE A S, DE POMERAI D I, et al. Construction and evaluation of a transgenic hsp16GFPlacZ Caenorhabdits elegans strain for environmental monitoring[J]. Environ Toxicol Chem, 2003,22:111118.
[22] WANG Y, XIE W, WANG D Y. Transferable properties of multibiological toxicity caused by cobalt exposure in Caenorhabditis elegans[J]. Environ Toxicol Chem, 2007,26:24052412.
[23] SHEN L L, XIAO J, YE H Y, et al. Toxicity evaluation in nematode Caenorhabditis elegans after chronic metal exposure[J]. Environ Toxicol Pharmacol, 2009,28:125132.
[24] XIAO J, RUI Q, GUO Y L, et al. Prolonged manganese exposure induces severe deficits in lifespan, development and reproduction possibly by altering oxidative stress response in Caenorhabditis elegans[J]. J Environ Sci, 2009,21:842848.
[25] LI Y H, WANG Y, YIN L H, et al. Using the nematode Caenorhabditis elegans as a model animal for assessing the toxicity induced by microcystinLR[J]. J Environ Sci, 2009,21:395401.
[26] America Society for Testing and Materials. Standard guide for conducting laboratory soil toxicity tests with the nematode Caenorhabditis elegans [M] // Annul book of ASTM standard. Philadelphia: PA, 2002,16061616.
[27] LORENZON S, FRANCESE M, FERRERO E A. Heavy metal toxicity and differential effects on the hyperglycemic stress response in the shrimp Palaemon elegans[J]. Arch Environ Cont Toxicol, 2000,39:167176.
[28] BRENNER S. The genetics of Caenorhabditis elegans[J]. Genetics, 1974,77:7194.
[29] DONKIN S, WILLIAMS P L. Influence of developmental stage, salts and food presence on various end points using Caenorhabditis elegans for aquatic toxicity testing[J]. Environ Toxicol Chem, 1995,14:21392147.
[30] SHEN L L, WANG Y, WANG D Y. Involvement of genes required for synaptic function in aging control in C. elegans[J]. Neurosci Bull, 2007,23:2129.
[31] HU Y O, WANG Y, YE B P, et al. Phenotypic and behavioral defects induced by iron exposure can be transferred to progeny in Caenorhabditis elegans[J]. Biomed Environ Sci, 2008,21:467473
[32] SWAIN S C, KEUSEKOTTEN K, BAUMEISTER B, et al. C. elegans metallothioneins: new insights into the phenotypic effects of cadmium toxicosis[J]. J Mol Biol, 2004,341:951959.
[33] TSALIK E L, HOBERT O. Functional mapping of neurons that control locomotory behavior in Caenorhabditis elegans[J]. J Neurobiol, 2003,56:178197.
[34] WANG D Y, XING X J. Assessment of locomotion behavioral defects induced by acute toxicity from heavy metal exposure in nematode Caenorhabditis elegans[J]. J Environ Sci, 2008,20:11321137.
[35] XING X J, GUO Y L, WANG D Y. Using the larvae nematode Caenorhabditis elegans to evaluate neurobehavioral toxicity to metallic salts[J]. Ecotoxicol Environ Safety, 2009,72:18191823.
[36] SAEKI A, YAMAMOTO M, LINO Y. Plasticity of chemotaxis revealed by paired presentation of a chemoattractant and starvation in the nematode Caenorhabditis elegans[J]. J Exp Biol, 2001,204:17571764.
[37] POPHAM J D, WEBSTER J M. Ultrastructural changes in C. elegans(Nematoda) caused by toxic levels of mercury and silver[J]. Ecotoxicol Environ Safe, 1982,6:183189.
[38] POWER R S, de POMERAI D I. Effect of single and paired metal inputs in soil on a stressinducible transgenic nematode[J]. Arch Environ Contam Toxicol, 1999,37:503511.
[39] XING X J, DU M, XU X M, et al. Exposure to metals induces morphological and functional alteration of AFD neurons in nematode Caenorhabditis elegans[J]. Environ Toxicol Pharmacol, 2009,28:104110.
[40] GUO Y L, YANG Y C, WANG D Y. Induction of reproductive deficits in nematode Caenorhabditis elegans exposed to metals at different developmental stages[J]. Reprod Toxicol, 2009,28:9095.
[41] SHIMADA H, TOMINAGA N, KOHRA S, et al. Metallothionein gene expression in the larvae of Caenorhabditis elegans is a potential biomarker for cadmium and mercury[J]. Trace Elem Electroly, 2003,20:240243.
心理学研究表明,兴趣是一种由于机体需要而产生的稳定的内驱力,是构成动机的最现实、最活跃的成分,是学习入门和获得成功之间的“牵引力”与“粘合剂”。如果我们地理教师善于寓教于乐,使教学活泼生动,情趣横生,培养和激发学生的“痴”情“迷”劲,使之欲罢不能,乐于探索,那么,不仅大大有益于提高当前地理教学效果,而且可能在学生心中埋下终身为之探索的种子。当然,在地理教学中,教师不能满足于对学生一讲就懂,更应善于提出新颖的引起认知冲突的问题,使学生产生浓厚的学习兴趣。举个例子来讲,初中地理教材涉及“时区及日界线”内容,学生接受起来有一定的困难,教师不妨在上课之初,首先向全班学生展示两个小问题:(1)“小华得知到日本东京访问的爸爸,今天就要回上海了,他了解到飞机从东京起飞的时间为早上8点,按照飞机飞行2小时15分钟计算,到达上海的时间应为10时15分。他准备到机场迎接爸爸。可是还没有动身呢,爸爸就回家了。这是怎么一回事呢?”(2)“一对孪生姐妹,姐姐先出生,但年龄小一岁,妹妹后出生,年龄却比姐姐大一岁。你知道这种奇妙情况的原因吗?”这样一来,学生就会带着强烈的好奇心来听老师讲课,并把这种兴趣转化为内在的学习动力。
二、创设“问题情境”,提倡探究教学
所谓设置“问题情境”,就是在教材内容与学生求知心理之间创造一种“不协调”,把学生引入一种与问题有关情境中的过程,这个过程也就是不协调――探究――发现――解决问题的过程。
在地理教学中,教师不要急于把现成的知识硬灌给学生,而要善于启发学生,帮助他们提高分析问题和解决问题的能力。要善于联系新旧知识间的相似点和不同点,引导学生充分利用已学知识探求新的知识。要根据教材内容和学生的认识水平,尽可能地创造条件,使学生通过观察、分析、总结,形成他们自己的概念。如在讲述北美气候部分时,首先要求学生阅读相关教材插图,然后设问:“北美与欧洲西部纬度相当,欧洲西部的气候表现了海洋性特征,而北美却普遍有大陆性特征,为什么?”学生只有通过比较、综合,才能得出确切的回答。当然,教师的提问不要过于频繁,如果把“弦”绷得过紧,而不让学生有思考回旋的余地,急于点“将”,让学生仓促上阵,很可能“卡壳”,从而影响学生的学习情绪。
三、打破“思维定势”,鼓励学生标新立异
在地理教学中,教师如果把学生的思维束缚在教科书的框框内,不准他们越雷池一步,那么只能使学生的思维活动处于一种“休眠”状态,结果扼杀了学生的首创精神。如何使学生认真学好前人的知识,既不受其拘束,敢于另辟蹊径,又能言之有理,持之有故,这就必须鼓励学生标新立异,打破“思维定势”,从而发现新问题,提出新设想。但是教师应该注意到,对学生的问题要推迟判断,避免武断。过早地下结论或向学生预示解决方法,都不利于创造思维的培养。即使学生把答案搞错了,也不必大惊小怪,要善于区分“笨拙的错误”和“创造性的错误”。后者往往是成功的先导,应当引起教师的重视。有位老师讲高中地理“生态系统”时,有学生问:“假若生态系统中没有微生物起作用,地球上还有没有生物?”尽管这位老师始料未及,但对学生敢于提问的做法予以了肯定。并要求同学们就此展开讨论,促使学生形成一种特殊的求异心理状态,鼓励学生深刻回味,大胆设疑,细心思考,据理力争。