Knockout Mice Download Ebook PDF Epub Online

Author : Jacqueline N. Crawley
Publisher : Wiley-Liss
Release : 2000-04-13
Page : 329
Category : Nature
ISBN 13 :
Description :


"Turn to What's Wrong With My Mouse? to discover the wealth of mouse behavioral tasks and to get the guidance you need to select the best methods and necessary controls. Chapters are organized by behavioral domain, including measurements of general health, motor functions, sensory abilities, learning and memory, feeding and drinking, reproductive, social, emotional, and reward behaviors in mutant mice. Throughout the chapters, new behavioral tasks and new research discoveries have been added, bringing the second edition up to date with the latest science." "Throughout the book, the use of behavioral testing equipment is illustrated with photographs, diagrams, and representative data, Examples of behavioral tasks successfully applied to transgenic and knockout mouse models are provided, as well as references to the primary literature and step-by-step methods protocols. These features, along with a comprehensive index, listings of database and vendor Web sites, suggestions for expert behavioral neuroscientist collaborators, and an extensive list of references, make this book a valuable and practical resource for students and researchers."--BOOK JACKET.


Author : J M Fulgham
Publisher : iUniverse
Release : 2008-02
Page : 176
Category : Fiction
ISBN 13 : 0595471811
Description :


Dr. Jonathan Goodman is desperate to cure his son Daniel's cancer. His wife, Lilith, becomes pregnant with another child, a sibling whose DNA can potentially cure Daniel. Their hopes are dashed when a genetic disorder is detected in their unborn child. When Daniel dies and their unborn child miscarries, grief and devastation splinter the couple's bond. Under emotional duress but driven to honor Daniel's memory, Jonathan, a brilliant medical researcher, makes a major breakthrough using genetically modified laboratory mice. He develops a novel treatment for several disease clusters, including cancer. Bypassing all protocols to push his findings forward, Goodman unethically secures approval and funding for a human clinical trial. With enough funding for four participants, Goodman carefully chooses those upon whom he'll experiment. Each participant faces a terminal illness, and Dr. Goodman's exploratory treatment is their last hope for survival. Despite his noble intentions, Goodman is motivated to exorcise the demons that haunt him. Those spirits, however, also besiege each member of the clinical trial. Lives will be forever changed-and possibly lost. Saving those whom Goodman has put in harm's way and saving what is left of his family and career presents an almost insurmountable challenge.


Author : Jacqueline N. Crawley
Publisher : John Wiley & Sons
Release : 2007-05-11
Page : 544
Category : Science
ISBN 13 : 0470119047
Description :


Dr. Jacqueline N. Crawley, author of the First and Second Editions of What’s Wrong with My Mouse? Behavioral Phenotyping of Transgenic and Knockout Mice,continues to field calls and e-mails from molecular geneticists who ask: how do I run behavioral assays to find out what’s wrong with my mouse? Turn to What’s Wrong with My Mouse? to discover the wealth of mouse behavioral tasks and to get the guidance you need to select the best methods and necessary controls. Chapters are organized by behavioral domain, including measurements of general health, motor functions, sensory abilities, learning and memory, feeding and drinking, reproductive, social, emotional, and reward behaviors in mutant mice. Throughout the chapters, new behavioral tasks and new research discoveries have been added, bringing the Second Edition up to date with the latest science. In addition, the Second Edition includes two new chapters: "Neurodevelopment and Neurodegeneration" discusses mouse behavioral tasks relevant to neurodevelopmental diseases, such as mental retardation and autism, and to neurodegenerative diseases, such as Alzheimers, Parkinsons, Huntingtons, and amyotrophic lateral sclerosis. "Putting It All Together" recommends strategies for optimizing a battery of behavioral phenotyping tests to address your specific hypotheses about gene functions. The final chapter, "The Next Generation," examines new and emerging technologies. Throughout the book, the use of behavioral testing equipment is illustrated with photographs, diagrams, and representative data. Examples of behavioral tasks successfully applied to transgenic and knockout mouse models are provided, as well as references to the primary literature and step-by-step methods protocols. These features, along with a comprehensive index, listings of database and vendor websites, and an extensive list of references, make this book a valuable and practical resource for students and researchers.


Author : Jerry J. Buccafusco
Publisher : CRC Press
Release : 2000-08-29
Page : 352
Category : Medical
ISBN 13 : 1420041819
Description :


Using the most well-studied behavioral analyses of animal subjects to promote a better understanding of the effects of disease and the effects of new therapeutic treatments on human cognition, Methods of Behavior Analysis in Neuroscience provides a reference manual for molecular and cellular research scientists in both academia and the pharmaceutic


Author : Jeroen Declercq
Prof. Dr. J.W.M. Creemers
Publisher : Biota Publishing
Release : 2012-10-01
Page : 30
Category : Science
ISBN 13 : 1615045260
Description :


The proprotein convertase Furin is a serine endoprotease which cleaves protein precursors carboxyterminal of basic residues in motifs such as Arg–X–X–Arg and Lys/Arg–Arg. Cleavage usually results in activation of the proprotein but can also inactivate or modify the activity. Therefore, it is not surprising that it plays a major role in many physiological processes and pathologies, including cancer. The other proprotein convertases belonging to the same family, PC1/3, PC2, PACE4, PC4, PC5/6, and PC7, cleave at similar cleavage sites and provide partial redundancy. To unravel the specific role of Furin in vivo, knockout mouse models have been generated. Furin null mice die between e10.5 and e11.5 due to severe ventral closure defects and the failure of the heart tube to fuse and undergo looping morphogenesis. Therefore, a conditional Furin knockout mouse was generated to investigate the role of Furin in specific organs, such as pancreas, liver, T-cells, endothelial cells, and salivary glands, resulting in a severe or mild phenotype depending on the organ investigated. Partial or complete ablation of the Fur gene in salivary gland tumors significantly delayed tumorigenesis in mice. Therefore, Furin inhibition might be considered as a possible therapeutic strategy to treat certain pathologies, such as cancer.


Author : Marc Adam Weiskopf
Publisher :
Release : 2005
Page : 64
Category :
ISBN 13 :
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Author : Ji-sook Moon (d)
Publisher :
Release : 2006
Page : 350
Category :
ISBN 13 :
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Author :
Publisher :
Release : 2005
Page : 17
Category :
ISBN 13 :
Description :


As the use of gene knockout models in thermoregulation studies has gained popularity, the reported incidence of redundant or discrepant phenotypes between studies has also increased, Several gene knockout models mimic human processes and have provided valuable insight into the role of endogenous mediators in thermoregulatory processes. There are also many examples of mutant strains expressing virtually identical phenotypes as their wild-type controls, causing concern regarding the appropriateness of these models for the study of physiological processes. In some cases, discrepancies in results are being reported from different laboratories that are studying the same gene knockout model. While mutant strains provide a powerful tool for analysis of gene function in vivo, the breeding strategies used to generate the strain may have a profound impact on the expressed phenotype. This review examines the intricacies of working with a small rodent such as the mouse and discusses the advantages and disadvantages of using gene knockout models for thermoregulatory research. A number of experimental strategies that can be used to minimize the occurrence of redundant phenotypes are presented. The influence of background strain effects is also considered, since this may be one of the most influential factors influencing a mutant phenotype. A future perspective is provided in which more advanced technologies using conditional gene inactivation and the production of rat knockout strains will improve current experimental design.


Author : Giamila Fantuzzi
Publisher : Springer Science & Business Media
Release : 2003-07-30
Page : 471
Category : Medical
ISBN 13 : 1592594050
Description :


Carrying on the high standards of the much praised first edition (Durum and Muegge, Cytokine Knockouts, 1998), Giamila Fantuzzi and a panel of experts have generated completely new chapters to reflect the use of many novel mouse strains and the hundreds of recent studies on cytokine physiology. Comprehensive reviews of the numerous often-surprising results obtained using cytokine knockout mice are provided, along with much important information about cytokine biology and physiology. For those not familiar with cytokine research, the authors present a critical discussion of the advantages and disadvantages of using cytokine knockout mice in various fields of research.


Author : James Calder
Tina L. Seelig
Publisher : Chronicle Books
Release : 2002
Page : 272
Category : Juvenile Nonfiction
ISBN 13 : 9780811834742
Description :


Packed with fun and fascinating facts, this card deck turns the world of bugs into games for your brain! Play creepy-crawly versions of Crazy Eights, Gin Rummy, Go Fish, Solitaire and Concentration, as you learn all about some of the coolest creatures that ever walked the earth.


Author : Scott K. Durum
Kathrin Muegge
Publisher : Springer Science & Business Media
Release : 2013-04-17
Page : 482
Category : Medical
ISBN 13 : 1475727534
Description :


My personal history in the field of cytokines had an initial period of several years during which my student and then colleague, Werner Muller, tried in vain to attract me to them. My interest always vanished when I was confronted with complex data pointing to func tional redundancy of cytokines in cell culture systems. When gene targeting in the mouse germline became possible, this frustration came to an end. We and others immediately embarked on analyzing the in vivo function of cytokines and the problem of functional redundancy with this powerful new approach. The early cytokine gene knockouts performed by colleagues in Wiirzburg (IL-2) and by ourselves (IL-4 and IL-l 0) seemed to give clear answers and at the same time led to surprises: Each of these cytokines apparently had its own special and irreplaceable function, and this function could be quite distinct from what had been anticipated from functional experiments in vitro. Al though the latter finding is of course a wonderful incentive for fur ther research, the former is pleasing in a general sense since it highlights the value of each of those one hundred thousand genes or so in our genome, cherished by evolution to become respectable mem bers of the community. Even in the present era of "genomics" there will be no way around the careful functional analysis of each gene by itself.


Author : Shree Ram Singh
Robert M. Hoffman
Publisher : Humana
Release : 2021-02-20
Page : 217
Category : Science
ISBN 13 : 9781071610077
Description :


This fully updated edition provides selected mouse genetic techniques and their application in modeling varieties of human diseases. The chapters are mainly focused on the generation of different transgenic mice to accomplish the manipulation of genes of interest, tracing cell lineages, and modeling human diseases. Written for the highly successful Methods in Molecular Biology series, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Authoritative and up-to-date, Mouse Genetics: Methods and Protocols, Second Edition delivers fundamental techniques and protocols to geneticists, molecular biologists, cell and developmental biologists, students, and postdoctoral fellows working in the various disciplines of genetics, developmental biology, mouse genetics, and modeling human diseases.


Author : Mariya Stavnichuk
Publisher :
Release : 2020
Page :
Category :
ISBN 13 :
Description :


"Bone and bone marrow tissues are not only anatomically, but also functionally interdependent. Conditions that affect bone marrow often result in extensive changes in bone architecture. Numerous studies demonstrated that an increase in the number of megakaryocytes in the bone marrow leads to osteosclerotic changes in the skeleton. Further, premature formation and activation of platelets have been recently shown to be inhibited by the G6b-B receptor located on megakaryocytes and platelets. Global knockout of the G6b-B receptor in mice leads to an elevated number of megakaryocytes in the bone marrow and myelofibrosis, a disorder commonly accompanied by osteosclerosis. Moreover, a group of patients with loss-of-function mutations in the G6b gene was identified to develop focal myelofibrosis. Therefore, we hypothesize that knockout of G6b-B will lead to osteosclerotic changes in the skeleton. We evaluated differences in spleen morphology and bone architecture in the G6b-B wildtype and global knockout mice at 4, 8, 16, and 32 weeks-of-age. Female G6b-B knockout mice developed splenomegaly evident from 8 weeks-of-age that was linked to an increase in the expression of erythropoietic markers. Micro-computed tomography analysis revealed that starting from 8 weeks, female G6b-B knockout mice developed progressive osteosclerosis of the femur that occluded the medullary cavity completely by 32 weeks-of-age. The progression of osteosclerosis was accompanied by an increase in the markers of osteoblast differentiation and a decrease in the markers of osteoclast activity suggesting an imbalance between bone formation and resorption. A comparison of the bone phenotype in mice with a global and megakaryocyte-lineage specific G6b-B knockout revealed that osteosclerosis was caused by the absence of G6b-B in megakaryocytes. Ovariectomy of global G6b-B knockout mice demonstrated that the development of osteosclerosis was not only linked to an elevated megakaryocyte level but also to estrogen levels. On the other hand, male G6b-B knockout mice did not develop splenomegaly or osteosclerosis of the femur but displayed reduced bone mass in the lumbar vertebrae. Further elucidation of the signaling pathways involved in megakaryocyte-mediated bone gain is important for the future design of treatments against osteosclerosis observed in patients with myelofibrosis or bone loss characteristic to osteoporosis"--


Author : Jennifer Lynn Daigle
Publisher :
Release : 2001
Page : 224
Category :
ISBN 13 :
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Author : Wing-On Tse
謝永安
Publisher :
Release : 2017-01-26
Page :
Category :
ISBN 13 : 9781360979953
Description :


This dissertation, "Hepatic Oxidative Stress in COX-1 Knockout Mice" by Wing-on, Tse, 謝永安, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. DOI: 10.5353/th_b4501095 Subjects: Oxidative stress Cyclooxygenases Liver - Diseases - Genetic aspects


Author : Ellafi A. E. Mohamed
Publisher :
Release : 2008
Page : 40
Category : Acetylcholine
ISBN 13 :
Description :



Author : Rebecca Jeanette Ralph
Publisher :
Release : 2001
Page : 482
Category :
ISBN 13 :
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Author : Pui-Chi Lee
李佩芝
Publisher : Open Dissertation Press
Release : 2017-01-26
Page :
Category :
ISBN 13 : 9781361340134
Description :


This dissertation, "Phenotypic Characterization of Adipocyte Fatty Acid Binding Protein Knockout Mice Under High Fat High Cholesterol Diet-induced Obesity" by Pui-chi, Lee, 李佩芝, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Background and objectives: A lot of studies proved that adipocyte fatty acid binding protein (A-FABP), an adipokine mainly expressed in adipocytes and macrophages, is the key link between obesity and inflammation which is suggested to be a therapeutic target for obesity-related diseases. Loss-of-function study was employed by using A-FABP knockout (KO) mice generated by our group to investigate role of A-FABP in high fat high cholesterol (HFHC) diet-induced obesity. Key findings: 1. Our study confirmed that HFHC diet-induced A-FABP KO mice have a significantly increased body weight when compared to the wild-type (WT) control mice. 2. Higher adiposity was the major reason for the A-FABP KO mice to be heavier than the WT controls under HFHC diet induction. 3. The marked increase of the weight of subcutaneous fat and peri-renal fat contributed to the higher adiposity of the HFHC-diet induced A-FABP KO mice when compared to the WT controls. 4. The HFHC-diet induced A-FABP KO mice significantly consumed less oxygen and produced less carbon dioxide suggesting the reduced energy expenditure but had higher weekly energy intake when compared with the WT controls, leading to higher adiposity. 5. The A-FABP KO mice were protected against HFHC diet induced glucose intolerance, insulin resistance, hyperglycemia and hyperinsulinemia when compared with the WT controls. There was also a better insulin secretion in response to glucose stimulation in A-FABP KO mice under prolonged HFHC diet induction when compared with the WT controls. 6. The A-FABP KO mice were protected against the development of hypercholesterolemia and hypertriglycemia when compared the WT controls under HFHC diet induction. However, there was no significant difference in the fasting serum free fatty acids (FFA) level among A-FABP WT and KO mice fed with standard chow (STC) or HFHC diet. 7. A-FABP KO mice were protected against isolated systolic hypertension (ISH) under HFHC diet induction. 8. The A-FABP KO mice were protected against HFHC diet-induced liver injury as indicated by a lower serum ALT level suggesting a better liver function when compared with the WT controls. 9. Under HFHC diet induction, M1 macrophage polarization was dominant in fat tissues of A-FABP WT mice but M2 macrophage polarization was dominant in fat tissues of A-FABP KO mice, suggesting an improved inflammatory status in the adipose tissue of the A-FABP KO mice when compared with the WT controls. This may also be the reason for why HFHC diet-induced A-FABP KO mice have an increased body weight but are metabolically healthier compared to their WT controls. Conclusions: A-FABP KO mice had a significant higher body weight and higher adiposity due to the reduced energy expenditure and increased weekly food intake as indicated in the metabolic cage study and the reason for metabolic healthier is due to the alleviated HFHC diet induced M1 macrophage polarization in various adipose tissues suggesting an improved inflammatory status in A-FABP KO mice comparing to the WT controls. DOI: 10.5353/th_b5194748 Subjects: Cytokines Fat cells Adipose tissues Obesity - Animal models


Author : Edward D. Levin
Jerry J. Buccafusco
Publisher : CRC Press
Release : 2006-06-22
Page : 400
Category : Science
ISBN 13 : 1420004336
Description :


The costs associated with a drug’s clinical trials are so significant that it has become necessary to validate both its safety and efficacy in animal models prior to the continued study of the drug in humans. Featuring contributions from distinguished researchers in the field of cognitive therapy research, Animal Models of Cognitive Impairment examines some of the most popular and successful animal archetypes used in the context of drug discovery. It provides integrated coverage of the latest research concerning neuronal systems relevant to cognitive function and dysfunction, assimilating reviews of this research within the context of each chapter. This approach is unique in that it brings together molecular and neurochemical methodologies, behavioral applications in translational models, and clinical applications. The book comprehensively discusses a wide variety of animal models of cognitive impairment, including genetic, lesion, pharmacological, and aging related impairments. It also explores the significance of this research in regards to the treatment of various addictions and disorders such as stroke, autism, Alzheimer’s, schizophrenia, and ADHD. Edited by two renowned authorities in the field, Animal Models of Cognitive Impairment is a timely book that provides integrated coverage of cutting-edge research that concerns neuronal systems relevant to cognitive function and dysfunction.


Author : David Stephen Margolis
Publisher :
Release : 2008
Page : 314
Category :
ISBN 13 :
Description :


Since the development of knockout and transgenic mouse models, mice have become the most widely used mammalian animal model to study bone. Despite the advances in knowledge of bone biology and function that have occurred from use of mouse models, many studies use primarily qualitative techniques, which may result in overlooking important subtle pathophysiologic changes. The hypothesis of this dissertation is that quantitative techniques to measure bone structure and function could identify the physiologic role of carbonic anhydrase II and calbindin-D28k in mouse bone, despite earlier qualitative studies indicating mice without these proteins have normal bone structure and function. Furthermore, a method to quantify bone function in vivo will be tested in a mouse model. Although carbonic anhydrase II deficient mice are less severely affected than patients, the mice demonstrate features of osteopetrosis including metaphyseal widening and a 50% increase in trabecular bone volume. The mice partially compensate for inhibited osteoclast function by increasing osteoclast number. Calbindin-D28k knockout mice demonstrated an increase in bone volume that results from additional bone at the endosteal surfaces. The higher bone volume results in increased stiffness and failure loads, highlighting the potential use of drugs that inhibit calbindin-D28k to treat diseases such as osteoporosis. Finally, calcium phosphate ceramic and hydroxyapatite particles used as strain gauge coatings demonstrated bone bonding to mouse femora after two months in vivo. The use of hydroxyapatite particles to coat strain gauges is the first time this method has been used with all commercially available materials, and will allow other research groups to use this technique. The major limitation to in vivo bone strain measurement in mice is the relatively large size of the sensors, which resulted in increased second moments of inertia in the implanted bones. Overall, this dissertation demonstrates that the use of quantitative techniques, including histology, histomorphometry, æ̐CT imaging, and mechanical testing can measure subtle changes in bone properties that have been previously overlooked. Development of additional quantitative methods to study bone biomechanics in mouse models may encourage other research groups to quantify bone properties if no changes are noted using primarily qualitative methods.