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INTEGRATION OF COMPUTER SIMULATION INTO THE COMMUNITY COLLEGE GENERAL BIOLOGY LABORATORY
Title
THE INTEGRATION OF COMPUTER SIMULATION INTO THE COMMUNITY COLLEGE GENERAL BIOLOGY LABORATORY.
Creator
MILLER, DARYL GILSON., Florida Atlantic University
Abstract/Description
The pedagogical effectiveness of the integration of computer-assisted instruction (CAI) into the community college general biology laboratory was compared with that of traditional "hands on" biology laboratory instruction. Two evaluative instruments were used as a measure of student achievement: a multiple choice test (pretest/posttest format) and a laboratory report form. The multiple choice posttest was readministered at a later date as an indicator of learning retention. Both evaluative...
Show moreThe pedagogical effectiveness of the integration of computer-assisted instruction (CAI) into the community college general biology laboratory was compared with that of traditional "hands on" biology laboratory instruction. Two evaluative instruments were used as a measure of student achievement: a multiple choice test (pretest/posttest format) and a laboratory report form. The multiple choice posttest was readministered at a later date as an indicator of learning retention. Both evaluative instruments were referenced as to higher and lower cognitive learning skills according to Bloom's Taxonomy and subscores for each category were obtained. Student pre- and post-attitude toward CAI was addressed through the administration of a CAI attitude inventory. Enzyme Investigations, a program developed for HRM Software by James Chandler (1985) was used in this study. Statistical comparisons consisted of either ANOVA or multifactor ANOVA with the level of rejection at 0.05. CAI students did not differ at either cognitive level of learning achievement from traditionally instructed lab students when measured with a multiple choice test. A significant difference was noted favoring CAI students for higher cognitive level learning as measured by a laboratory report. Gender differences favoring male CAI students approached significance (p = 0.0759) using the multiple choice test but comparable differences were not noted with lab report scores. When test scores of students at varying levels of academic achievement (as measured by grade point average) were compared, the CAI and traditional groups' performances were similar for both evaluative instruments. No significant difference was noted between the CAI and traditional groups when learning retention was measured. Student participation in the CAI produced no significant change in attitude toward this instructional strategy. It was concluded that when the two forms of instruction were compared in the general biology laboratory, integrated CAI was at least as effective as traditional methods at the community college level. Additionally, CAI appears to be more effective than traditional lab methods for teaching higher level cognitive skills.
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Date Issued
1986
PURL
http://purl.flvc.org/fcla/dt/11883
Subject Headings
Computer-assisted instruction, Biological laboratories, Community colleges
Format
Document (PDF)
Influence of small conductance calcium-activated potassium channels (SK,Kca2) on long-term memory
Title
Influence of small conductance calcium-activated potassium channels (SK,Kca2) on long-term memory: global and local analysis across time- and task- dependent measures.
Creator
Vick, Kyle A., Charles E. Schmidt College of Science, Department of Psychology
Abstract/Description
Small conductance calcium-activated potassium (SK) channels are found ubiquitously throughout the brain and modulate the encoding of learning and memory. Systemic injection of 1-ethyl-2-benzimidalzolinoe (EBIO), a SK channel activator, impairs the encoding of novel object memory and locomotion but spares fear memory encoding in C57BL/6NHsd mice. The memory impairments discovered were not due to non-cognitive performance confounds such as ataxia, anxiety, attention or analgesia. Further...
Show moreSmall conductance calcium-activated potassium (SK) channels are found ubiquitously throughout the brain and modulate the encoding of learning and memory. Systemic injection of 1-ethyl-2-benzimidalzolinoe (EBIO), a SK channel activator, impairs the encoding of novel object memory and locomotion but spares fear memory encoding in C57BL/6NHsd mice. The memory impairments discovered were not due to non-cognitive performance confounds such as ataxia, anxiety, attention or analgesia. Further investigation with intra-hippocampal application of EBIO revealed SK channels in dorsal CA1 contribute to the encoding deficits seen systemically, but do not account for the full extent of the impairment. Concentrated activation of dorsal CA1 SK channels do not influence fear memory encoding or locomotor impairments. Taken together, these data indicate SK channels, especially in the dorsal hippocampus, have a modulatory role on novel object memory encoding, but not retrieval; however, pharmacological activation of hippocampal SK channels does not appear to influence fear memory encoding.
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Date Issued
2009
PURL
http://purl.flvc.org/FAU/192991
Subject Headings
Mice as laboratory animals, Cellular signal transduction, Memory, Research, Biological transport, Research, Potassium channels, Physiological effect
Format
Document (PDF)
The effect of small conductance calcium-activated potassium channels on emotional learning and memory
Title
The effect of small conductance calcium-activated potassium channels on emotional learning and memory.
Creator
Sanguinetti, Shannon, Stackman, Robert W., Florida Atlantic University, Charles E. Schmidt College of Science, Department of Psychology
Abstract/Description
Small conductance Ca2+-activated K+ (SK) channels have been shown to alter the encoding of spatial and non-spatial memory in the hippocampus by shaping glutamatergic postsynaptic potentials and modulating NMDA receptor-dependent synaptic plasticity. When activated, dendritic SK channels reduce hippocampal neuronal excitability and LTP. Similar SK channel properties have been demonstrated in lateral amygdala (LA) pyramidal neurons. Additionally, induction of synaptic plasticity and beta...
Show moreSmall conductance Ca2+-activated K+ (SK) channels have been shown to alter the encoding of spatial and non-spatial memory in the hippocampus by shaping glutamatergic postsynaptic potentials and modulating NMDA receptor-dependent synaptic plasticity. When activated, dendritic SK channels reduce hippocampal neuronal excitability and LTP. Similar SK channel properties have been demonstrated in lateral amygdala (LA) pyramidal neurons. Additionally, induction of synaptic plasticity and beta-adrenoreceptor activation in LA pyramidal neurons causes PKA-mediated internalization of SK channels from the postsynaptic density. Chronic activation of the amygdala through repetitive stressful stimuli can lead to excitatory synaptic strengthening that may create permanent hyper-excitability in its circuitry. This mechanism may contribute to a number of mood and anxiety disorders. The selective influence of SK channels in the LA on anxiety and fear conditioning are not known. The thesis project outlined herein examined whether SK channel blockade by bee venom peptide, apamin, during a repetitive acute fear conditioning paradigm was sufficient to alter fear memory encoding and the resulting behavioral outcome. Following the final fear memory test session, mice were tested in the open field immediately after the second fear conditioning test session. The findings indicate that intracranial LA microinfusions of apamin did not affect memory encoding or subsequent anxiety.
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Date Issued
2015
PURL
http://purl.flvc.org/fau/fd/FA00004543, http://purl.flvc.org/fau/fd/FA00004543
Subject Headings
Biological transport -- Research, Cellular signal transduction, Memory -- Research, Mice as laboratory animals, Potassium channels -- Physiological effect
Format
Document (PDF)
response of rat retinal ganglion cells to axotomy: Early changes in the regulation of fast transported proteins
Title
The response of rat retinal ganglion cells to axotomy: Early changes in the regulation of fast transported proteins.
Creator
Wodarczyk, Linda, Florida Atlantic University, Perry, Gary W.
Abstract/Description
Mammals, unlike lower vertebrates, cannot normally regenerate injured central nervous system neurons. Although rat retinal ganglion cells (RGCs), following optic nerve crush, will undergo an initial period of sprouting, axon outgrowth is limited and subsequently aborted. This study examined how extensive the changes in fast transported proteins (FTPs) were during the early response to RGC damage and whether these changes were comparable to those known to occur in lower vertebrate RGCs....
Show moreMammals, unlike lower vertebrates, cannot normally regenerate injured central nervous system neurons. Although rat retinal ganglion cells (RGCs), following optic nerve crush, will undergo an initial period of sprouting, axon outgrowth is limited and subsequently aborted. This study examined how extensive the changes in fast transported proteins (FTPs) were during the early response to RGC damage and whether these changes were comparable to those known to occur in lower vertebrate RGCs. Changes in mRNA for several known proteins were also analyzed. It was found that, within 2 days, axotomized rat RGCs initiated a program of cell growth, involving the differential synthesis and transport of a broad range of FTPs. This response is very similar to that of lower vertebrates and indicates that rat RGCs are capable of initiating the metabolic responses necessary for regeneration to begin. This response, however, was not sustained beyond 5 days axotomy.
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Date Issued
1994
PURL
http://purl.flvc.org/fcla/dt/15074
Subject Headings
Regeneration (Biology), Retinal ganglion cells, Rats as laboratory animals, Nerves--Growth
Format
Document (PDF)
cTnI N-Terminal deletion: an agent for rescuing restrictive cardiomyopathy, a disease caused by mutations of Cardiac Troponin I
Title
cTnI N-Terminal deletion: an agent for rescuing restrictive cardiomyopathy, a disease caused by mutations of Cardiac Troponin I.
Creator
Getfield, Cecile A., Huang, Xupei, Florida Atlantic University, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description
Restrictive cardiomyopathy (RCM) is represented in part by left ventricular stiffness and diastolic dysfunction. Missense mutations of the cardiac troponin I (cTnI) gene cause idiopathic RCM. These mutations are located in the C-terminus of cTnI and affect cardiac relaxation. Transgenic mouse models presenting the pathology observed in clinical patients with RCM have been generated previously and express the mutant cTnI in their hearts. RCM-linked mutations increase cardiac myofilament Ca2+...
Show moreRestrictive cardiomyopathy (RCM) is represented in part by left ventricular stiffness and diastolic dysfunction. Missense mutations of the cardiac troponin I (cTnI) gene cause idiopathic RCM. These mutations are located in the C-terminus of cTnI and affect cardiac relaxation. Transgenic mouse models presenting the pathology observed in clinical patients with RCM have been generated previously and express the mutant cTnI in their hearts. RCM-linked mutations increase cardiac myofilament Ca2+ sensitivity and promote diastolic dysfunction in the heart. Previous studies using double transgenic mice (cTnI/R193H/ND) showed that ventricular relaxation is enhanced in the cTnI/R193H transgenic mice. In this study, another double transgenic mouse model, (cTnI/R193H/ND/KO), provides an avenue to investigate its rescuing effects on RCMlinked mutations in the cTnI /R193H/KO mouse. Use of molecular biological techniques, transgenic animal developments and murine echocardiography in this study has culminated into a greater understanding of RCM and diastolic dysfunction.
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Date Issued
2014
PURL
http://purl.flvc.org/fau/fd/FA00004196, http://purl.flvc.org/fau/fd/FA00004196
Subject Headings
Biochemical markers -- Diagnostic use, Cardiovascular system -- Pathophysiology, Coronary heart disease -- Molecular diagnosis, Mice as laboratory animals, Molecular biology
Format
Document (PDF)
Mechanism and treatment of restrictive cardiomyopathy
Title
Mechanism and treatment of restrictive cardiomyopathy.
Creator
Jean-Charles, Pierre-Yves, Charles E. Schmidt College of Medicine, Department of Biomedical Science
Abstract/Description
Restrictive cardiomyopathy (RCM) is a cardiac muscle disorder characterized by increased ventricular stiffness and diastolic dysfunction. Patients with RCM often present severe cardiac problems which usually lead to heart failure and sudden death. No effective treatment is available for RCM which makes the finding of novel efficient therapies an urgent necessity. Great progress in molecular biology techniques and advances in transgenic animal development provide great opportunities for the...
Show moreRestrictive cardiomyopathy (RCM) is a cardiac muscle disorder characterized by increased ventricular stiffness and diastolic dysfunction. Patients with RCM often present severe cardiac problems which usually lead to heart failure and sudden death. No effective treatment is available for RCM which makes the finding of novel efficient therapies an urgent necessity. Great progress in molecular biology techniques and advances in transgenic animal development provide great opportunities for the study of RCM and other cardiovascular diseases encountered in clinical patients.... Our laboratory is among the first to generate transgenic mouse models of RCM based on cardiac troponin I (cTnI) missense mutations. In this study, transgenic mice that suffer from RCM have been generated to understand the factors behind the diastolic dysfunction associated with that myocardial disease.... The information obtained from this study allows a better understanding of the role of troponin in RCM and the factors behind the physiopathology of the disease. It will also offer a therapeutic strategy taking into account the physiological characteristic of RCM.
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Date Issued
2012
PURL
http://purl.flvc.org/FAU/3358554
Subject Headings
Biochemical markers -- Diagnostic use, Cardiovascular system -- Pathophysiology, Coronary heart disease -- Molecular diagnosis, Mice as laboratory animals, Molecular biology
Format
Document (PDF)