案例在生物学复习教学中的应用

选择真实而有趣的案例，设计核心问题有针对性地系统地组织高考第2轮复习，能有效地激发学生的学习兴趣。提高学生对知识的提取应用和重构的能力。     

高三复习课中基于问题解决的反思和改进实践研究——以“染色体变异”一节为例

依照问题反思、学习研究、改进设计、实践总结的教学模式,对提高高三生物学复习课的高效性进行了实践探索,提高了复习课的针对性,取得了很好的复习效果。     

初试"问题情境式"复习法

随着综合科目考试的不断深化 ,综合科考试的“源于大纲 ,而不拘泥于大纲”、“重点考查学生的综合素质”等考查目标更现具体。处理好时间紧与课本知识点多、基础知识点复习与学生综合能力培养、学生知识面有限而考试命题涉及范围广等矛盾。是实现高三复习的高效、有序的保证。“问题情境式”复习方法 ,在过去两年的高三生物科复习中 ,取得了一定效果。1　“问题情境”式复习法的理论依据现代认知心理学关于思维的研究成果表明 ,思维过程首先是解决问题的过程 ,即思维通常是由问题情境产生的 ,而且以解决问题情境为目的。所谓问题情境是指个…     

深挖教材,利用生成性问题提高探究能力

教材和学生都是教师教学中重要的课程资源。以《酶的作用受许多因素的影响》的复习教学为例,通过深挖教材,同时关注学生在课堂上动态生成的问题,进行适当处置,培养学生实验探究能力和发散性思维,提高课堂教学的效果。     

关于高三第1轮复习方法的探讨

在整个高三1年的备考复习中,我们进行了以夯实基础知识为教学目标的第1轮复习;以提高学生能力．拓宽学生视野为目标的题型专题练习、实验专题练习和热点专题练习;以查漏补缺,增强学生自信心和提高学生应试能力为目标的冲刺模拟训练等3轮复习,以帮助学生理解、掌握生物学的基础知识,提高学生分析问题和解决问题的能力等,收到了良好的教学效果。     

以“问题驱动”为策略 优化高三复习教学

在"有丝分裂"复习教学中,通过鼓励学生主动提出问题、教师设计一定思维容量的问题及问题解决后所获得知识的迁移应用,让复习教学过程成为不断发现问题、分析问题和解决问题的过程,可以激发生成、发展知识、提升思维,从而提高复习效率。     

生物复习课课堂教学有效性的实验探索

在新课程背景下,如何在有限的时间内激发学生学业水平测试复习的积极性,提高复习效率,是生物教学一大难题。本文通过对学生实际情况分析,利用随堂评价的复习方式,编拟合适提纲和试题对学生进行教学和训练,关注最基础、核心的生物知识和学生学习情感,加强复习课验收、反馈、纠正环节等落实。新的复习教学方式,提高了复习效率,帮助学生找回学习的成就感和幸福感,激发学生学习生物的兴趣,提高学习积极性,同时也能提高教师自身素质,实践课堂教学的有效性。     

浅论探究性学习在高三生物专题复习课教学中的应用

在高三生物复习课教学中,如果只靠教师全面讲解,将所学知识机械地重复一遍,会让学生有“炒冷饭”的感觉。学生的学习兴趣和参与程度会大大降低,导致复习效率低下。因此,创造性地构建复习过程,与学生活跃的思维对接,提高复习效率,应是师生共同追求的目标。探究性学习是一种以问题为载体,以主动探究为特征的学习活动。教师要特别重视将探究性学习引入复习课,     

生物学教学中运用PBL方法的尝试--兼谈高中生物学一节复习课的教学

PBL(problem—based learning)是“以问题为基础”的教学模式,国外主要应用在临床医学的教学中。结合高中生物学一节课的复习教学,以糖尿病的研究为问题情境,以人类探索糖尿病和研究胰岛素的历史为线索进行教学设计,通过讨论问题的形式,帮助学生回忆和运用已有的知识,并使这节复习课的教学体现学生学习的主动性和探究性。最后简要总结了这种方法的优点和对生物学教学的适用性。     

高三生物第一轮复习应着重“六环节”

生物学科知识点多面广、而高三复习时间紧、任务重,新的高考又着重考查学生的创新精神和实践能力。如何有效地提高复习效率,使学生对平时所学知识系统化、概念化、完善化;培养其适应新的高考考试模式变化的能力,是每一个高三老师都在思索的问题。本人就抓好高三生物第一轮复习“六环节”谈一些看法。     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.