Lane Medical Library

Books by Subject

Biology

  • Digital
    Wilhelm Foissner, Kuidong Xu.
    Springer2006
    vol. 1. Protospathidiidae, Arcuospathidiidae, Apertospathulidae --
  • Digital
    by John B. Silver.
    Springer2008
    Designing a mosquito sampling programme -- Sampling the egg population -- Sampling the larval population -- Sampling the emerging adult population -- Sampling the adult resting population -- Sampling adults by animal bait catches and by animal-baited traps -- Blood-feeding and its epidemiological significance -- Sampling adults with non-attractant traps -- Sampling adults with light-traps -- Sampling adults with carbon dioxide traps -- Sampling adults with visual attraction traps, sound traps, and other miscellaneous attraction traps -- Estimation of the mortalities of the immature stages -- Methods of age-grading adults and estimation of adult survival rates -- Estimating the size of the adult population -- Measuring adult dispersal -- Experimental hut techniques -- Indices of association and species diversity indices.
  • Digital
    David J. K. Balfour, Marcus R. Munafò, editors.
    Springer2015
    The primary purpose of this book and its companion volume The Neuropharmacology of Nicotine Dependence is to explore the ways in which recent studies on nicotine and its role in tobacco addiction have opened our eyes to the psychopharmacological properties of this unique and fascinating drug. While the present volume considers the molecular and genetic factors which influence behavioral responses to nicotine and how these may impact on the role of nicotine in tobacco dependence, the book The Neuropharmacology of Nicotine Dependence focuses on the complex neural and psychological mechanisms that mediate nicotine dependence in experimental animal models and their relationship to tobacco addiction in humans. These volumes will provide readers with a contemporary overview of current research on nicotine psychopharmacology and its role in tobacco dependence from leaders in this field of research and will hopefully prove valuable to those who are developing their own research programmes in this important topic. CTBN Vol 23 The Behavioral Genetics of Nicotine and Tobacco The primary purpose of this book and its companion volume The Neuropharmacology of Nicotine Dependence is to explore the ways in which recent studies on nicotine and its role in tobacco addiction have opened our eyes to the psychopharmacological properties of this unique and fascinating drug. While the present volume considers the molecular and genetic factors which influence behavioral responses to nicotine and how these may impact on the role of nicotine in tobacco dependence, the book The Neuropharmacology of Nicotine Dependence focuses on the complex neural and psychological mechanisms that mediate nicotine dependence in experimental animal models and their relationship to tobacco addiction in humans. These volumes will provide readers with a contemporary overview of current research on nicotine psychopharmacology and its role in tobacco dependence from leaders in this field of research and will hopefully prove valuable to those who are developing their own research programmes in this important topic.
  • Digital
    edited by Robbin Gibb, Bryan Kolb.
    ScienceDirect2018
    The Neurobiology of Brain and Behavioral Development provides an overview of the process of brain development, including recent discoveries on how the brain develops. This book collates and integrates these findings, weaving the latest information with core information on the neurobiology of brain development. It focuses on cortical development, but also features discussions on how the other parts of the brain wire into the developing cerebral cortex. A systems approach is used to describe the anatomical underpinnings of behavioral development, connecting anatomical and molecular features of brain development with behavioral development. The disruptors of typical brain development are discussed in appropriate sections, as is the science of epigenetics that presents a novel and instructive approach on how experiences, both individual and intergenerational, can alter features of brain development. What distinguishes this book from others in the field is its focus on both molecular mechanisms and behavioral outcomes. This body of knowledge contributes to our understanding of the fundamentals of brain plasticity and metaplasticity, both of which are also showcased in this book.
  • Digital
    edited by Carla Mucignat-Caretta, Department of Molecular Medicine, University of Padova, Padova, Italy.
    CRCnetBASE2014
    Chapter 1. Introduction to chemical signaling in vertebrates and invertebrates / Tristram D. Wyatt -- chapter 2. Pheromones and general odor perception in insects / Michel Renou -- chapter 3. First investigation of the semiochemistry of South African dung beetle species / Barend (Ben) Victor Burger -- chapter 4. Pheromone reception in insects : the example of silk moths / Karl-Ernst Kaissling -- chapter 5. Chemical communication in the honey bee society / Laura Bortolotti and Cecilia Costa -- chapter 6. Drosophila pheromones : from reception to perception / Wynand van der Goes van Naters -- chapter 7. How drosophila detect volatile pheromones : signaling, circuits, and behavior / Samarpita Sengupta and Dean P. Smith -- chapter 8. Chemical signaling in amphibians / Sarah K. Woodley -- chapter 9. Vomeronasal organ : a short history of discovery and an account of development and morphology in the mouse / Carlo Zancanaro -- chapter 10. Vomeronasal receptors and signal transduction in the vomeronasal organ of mammals / Simona Francia, Simone Pifferi, Anna Menini, and Roberto Tirindelli -- chapter 11. Central processing of intraspecific chemical signals in mice / Carla Mucignat-Caretta -- chapter 12. Molecular and neural mechanisms of pheromone reception in the rat vomeronasal system and changes in the pheromonal reception by the maturation and sexual experiences / Makoto Kashiwayanagi -- chapter 13. Social cues, adult neurogenesis, and reproductive behavior / Paolo Peretto and Raúl G. Paredes -- chapter 14. Influence of cat odor on reproductive behavior and physiology in the house mouse (mus musculus) / Vera V. Voznessenskaya -- chapter 15. Pheromone of tiger and other big cats / Mousumi Poddar-Sarkar and Ratan Lal Brahmachary -- chapter 16. Cattle pheromones / Govindaraju Archunan, Swamynathan Rajanarayanan, and Kandasamy Karthikeyan -- chapter 17. Pheromones for newborns / Benoist Schaal -- chapter 18. Pheromone processing in relation to sex and sexual orientation / Ivanka Savic -- chapter 19. Human pheromones : do they exist? / Richard L. Doty.
  • Digital
    Susan L. Andersen, Daniel S. Pine, editors.
    Springer2014
    "Brain development, whether typical or atypical, provides the foundation for all behavior and possible psychopathology. This volume takes a comprehensive and translational approach in describing how basic neuronal patterning occurs, organizes into systems, and forms functional and inter-connected networks. The role that hormones and genes play in influencing brain development is also described. The resultant emotional, cognitive, reward, and social systems show how typical development proceeds. The second part of the book describes when the process of development goes awry. Here, a number of childhood disorders are covered. Autism, ADHD, emotional syndromes of bipolar disorder and depression, oppositional defiant disorder and conduct disorder, and sleep and schizophrenia are included in this volume. Written by leading experts in their respective fields, this volume will be a valuable resource to mental health professionals as well as preclinical investigators hoping to gain additional understanding about the neurobiology of the developing brain."--Publisher's website.
  • Digital
    edited by Andries Kalsbeek, Martha Merrow, Till Roenneberg, and Russell G. Foster.
    ScienceDirect2012
    This issue of Progress in Brain Research reviews current knowledge and understanding, provides a starting point for researchers and practitioners entering the field, and builds a platform for further research and discovery. Leading authors review the state-of-the-art in their field of investigation, and provide their views and perspectives for future research Chapters are extensively referenced to provide readers with a comprehensive list of resources on the topics covered All chapters include comprehensive background information and are written in a clear form that is also accessible to the non-specialist.
  • Digital
    edited by Quentin D. Wheeler.
    CRCnetBASE2008
    Introductory : toward the new taxonomy / Quentin D. Wheeler -- Networks and their role in e-taxonomy / Malcolm J. Scoble -- Taxonomy as a team sport / Sandra Knapp -- Planetary biodiversity inventories as models for the new taxonomy / Lawrence M. Page -- On the use of taxonomic concepts in support of biodiversity research and taxonomy / Nico M. Franz, Robert K. Peet and Alan S. Weakley -- International infrastructure for enabling the new taxonomy : the role of the Global Biodiversity Information Facility (GBIF) / Larry Speers and James L. Edwards -- DNA sequence in taxonomy : opportunities and challenges / Rudolf Meier -- Animal names for all : ICZN, ZooBank and the new taxonomy / Andrew Polaszek, Richard Pyle and Doug Yanega -- Understanding morphology in systematic contezxt : three-dimensional specimen ordination and recognition / Norman MacLeod -- Taxonomic shock and awe / Quentin D. Wheeler.
  • Digital
    edited by Lisa Plitnick, Danuta Herzyk.
    ScienceDirect2013
    Machine generated contents note: I.Development of Biophar-Maceuticals Defined as Novel Biologics -- 1.Overview of Biopharmaceuticals and Comparison with Small-molecule Drug Development / Thomas R. Gelzleichter -- Introduction -- History and Evolution of Biopharmaceuticals -- Development of Diverse Biopharmaceutical Modalities -- Comparison of Small-Molecule Drugs to Biopharmaceuticals -- Summary -- References -- 2.Regulatory Guidelines and their Application in the Nonclinical Evaluation of Biological Medicines / Maggie Dempster -- Introduction -- Species Selection -- Study Design Considerations for Repeat-Dose Studies -- Immunogenicity -- Reproductive and Developmental Toxicity -- Genotoxicity and Carcinogenicity -- Special Considerations for Anticancer Drugs -- First-in-Human (Fih) Clinical Trial -- Summary -- References -- 3.Early De-risking Strategy for Novel Biotherapeutics / Beth Hinkle -- Introduction -- Establishing A Safety Profile for Biotherapeutics -- General Safety Considerations Related to Biotherapeutics -- Progress in Evaluation of Immunotoxicity -- Can We Better Address Potential Off-Target Toxicity? -- Summary -- References -- 4.Novel Biopharmaceuticals: Pharmacokinetics, Pharmacodynamics, and Bioanalytics / Wolfgang Seghezzi -- Introduction -- Absorption, Distribution and Elimination of Biopharmaceuticals -- Disposition of Modified Molecules -- "Metabolism" and Biodistribution for Biopharmaceuticals -- Immunogenicity and impacts on PK and biodistribution -- Pharmacokinetics and Pharmacodynamics -- Preclinical to Clinical Translation -- Bioanalytics -- Drug Assays -- Biomarkers: Target Engagement Assays -- Immunogenicity Assessment: ADA Assays -- Summary -- References -- II.Development of Biosimilars -- 5.Overview of Biosimilar Therapeutics / Danuta J. Herzyk -- Introduction -- The Concept of Biosimilars -- General Considerations for Development of Biosimilars -- Biosimilar Candidates Based on Modality and Therapeutic Class -- Summary -- References -- 6.Regulatory Standards for the Approval of Biosimilar Products: A Global Review / Barbara Mounho-Zamora -- Introduction -- European Union -- Pioneer for the First Regulatory Pathway for Biosimilar Products -- The World Health Organization Guidance on Biosimilars -- Regulatory Pathway for Biosimilar Products in the United States -- Biosimilar Pathways in Other Regions -- Summary -- References -- 7.Early Characterization of Biosimilar Therapeutics / Thomas R. Gelzleichter -- Introduction -- Recombinant Insulins -- Recombinant Human Growth Hormone -- Recombinant Erythropoietins -- Recombinant Granulocyte Colony-Stimulating Factor -- Recombinant Interferons -- Low Molecular Weight Heparins -- Monoclonal Antibodies -- Other Classes -- Summary -- References -- III.Vaccines -- 8.Introduction to Vaccines and Adjuvants / Deborah L. Novicki -- Introduction -- The History of Vaccines -- The Impact of Vaccines on Human Health -- Advancements in Vaccines Technologies -- Advancements in Adjuvant Technologies -- Approved Infectious Disease Vaccines and Diseases for Which Preventive Vaccines are Still Needed -- Therapeutic Vaccines -- Product Complexity From a Quality Perspective -- Nonclinical Testing -- Clinical Testing -- Vaccine Development Using the Animal Rule -- The Anti-Vaccines Movement and Misperceptions About Vaccines and Their Safety -- Summary -- References -- 9.Global Regulatory Guidelines for Vaccines / Lisa M. Plitnick -- Introduction -- Toxicity Assessment -- Additional Toxicity Assessments -- Special Considerations -- Formulation/Delivery Devices -- Alternate Routes of Administration -- Special Considerations for Particular Types of Vaccines -- Summary -- References -- 10.Special Considerations for the Nonclinical Safety Assessment of Vaccines / Jayanthi J. Wolf -- Introduction -- De-risking Strategies for Vaccines -- Pharmacokinetics and Pharmacodynamics Assessments -- Differences in the Nonclinical Safety Assessment of Vaccines and Biopharmaceutical Drugs -- Summary -- References -- IV.Specialty Biologics and Indications -- 11.Turning the Corner with Viral-based Gene Therapy -- Development of the Rogue Biopharmaceutical / Timothy K. Maclachlan -- Introduction -- A History and Primer of Gene Therapy -- The Process of Getting Genes into Cells -- Health Authority Regulation of Gene Therapy Products -- Nonclinical Safety Studies and Regulatory Guidance -- Summary -- References -- 12.Blood Products / Vikram Arora -- Introduction -- Plasma-Derived Blood Products -- Blood Products Derived from Recombinant Technologies -- Summary -- References -- 13.Biological Therapies for Cancer / Gautham K. Rao -- Introduction -- Global Regulatory Guidances -- General Principles of Toxicology Assessments -- Nonclinical Studies and Principles of Study Design -- Specialty Toxicology Assessments -- Pharmacokinetics, Immunogenicity, and Pharmacodynamics -- Nonclinical Development of Marketed Biologies -- Recombinant Analogs of Endogeneous Human Proteins (Interferons, Cytokines, Enzymes) -- Summary -- References -- 14.Nonclinical Development of Multi-targeting Biopharmaceuticals / Anu V. Connor -- Introduction -- Scientific Rationale for Multi-Targeting Biopharmaceuticals (MTBs) -- Evolution of Technology Platforms -- General Challenges and Considerations -- Summary of Challenges -- T Cell-Dependent Bispecific Antibody (TDB) Biotherapeutics -- Dual-Targeting Antibodies -- Summary -- References -- 15.Considerations in the Development of Pluripotent Stem Cell-based Therapies / Joy A. Cavagnaro -- Introduction -- Early Decisions -- Nonclinical Development -- Translating Preclinical Data to Clinical Application -- Global Regulatory Guidance -- Summary -- References.
  • Digital
    by Andrii Rozhok.
    Springer2008
  • Digital
    Giuseppe Valacchi, editor ; Paul A. Davis, co-editor.
    Springer2008
  • Digital/Print
    edited by Helmut Sies and Bernard Brüne.
    Digital : ScienceDirect2007
    Print2007
  • Digital
    edited by Lars Olof Björn.
    Springer2008
  • Digital
    John A. Fuerst, editor.
    Springer2013
    History, classification and cultivation of the planctomycetes / Cheryl Jenkins and James T. Staley -- Cell compartmentalization and endocytosis in planctomycetes: structure and function in complex bacteria / John A. Fuerst, Richard I. Webb, and Evgeny Sagulenko -- Structural aspects of MC proteins of PVC superphylum members / Damien P. Devos -- Cell biology of anaerobic ammonium-oxidizing bacteria: unique prokaryotes with an energy-conserving intracellular compartment / Sarah Neumann, Muriel C.F. van Teeseling and Laura van Niftrik -- Acidophilic planctomycetes: expanding the horizons of new planctomycete diversity / Svetlana N. Dedysh and Irina S. Kulichevskaya -- Toward the development of genetic tools for Planctomycetes / Mareike Jogler and Christian Jogler -- Genomics and bioinformatics of the PVC superphylum / Olga K. Kamneva, Daniel H. Haft, Stormy J. Knight, Davide A. Liberles, and Naomi L. Ward -- Distribution and evolution of C1 transfer enzymes and evolution of the planctomycetes / Ludmila Chistoserdova -- Unusual members of the PVC superphylum: the methanotrophic Verrucomicrobia genus "Methylacidiphilum" / Christine E. Sharp, Huub J.M. Op den Camp, Ivica Tamas, and Peter F. Dunfield -- Phyla related to Planctomycetes: members of phylum Chlamydiae and their implications for Planctomycetes cell biology / Claire Bertelli and Gilbert Greub -- Planctomycetes: their evolutionary implications for models for origins of eukaryotes and the eukaryote nucleus and endomembranes / John A. Fuerst and Evgeny Sagulenko -- Final word: the future of planctomycetology and related studies / John A. Fuerst -- Index.
  • Digital
    Berryman, A. A.; Berryman, A. A.; Kindlmann, Pavel.
    Springer2008
  • Digital
    Peter Gluckman, Alan Beedle, Tatjana Buklijas, Felicia Low, Mark Hanson.
    OSO2016
  • Digital
    ScienceDirectv. 2-15, 1995-2004.
  • Digital/Print
    Jaroslava Halper, editor.
    Digital : Springer2014
    Print2014
    This volume is a reference handbook focusing on diseases like Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome and other heritable soft connective tissue diseases. The book presents detailed information for both basic scientists and for clinicians seeing patients. It is also a stepping stone for new investigations and studies that goes beyond the facts about the composition and biochemistry of the connective tissue and extracellular matrix, as the authors connect individual components to specific aspects of various soft tissue disorders and to the actual or potential treatment of them. Progress in Heritable Soft Connective Tissue Diseases features very prominent physicians and scientists as contributors who bring their most recent discoveries to the benefit of readers. Their expertise will help clinicians with proper diagnosis of sometimes elusive and uncommon heritable diseases of soft connective tissues. This book also offers an update on the pathophysiology of these diseases, including an emphasis on unifying aspects such as connections between embryonic development of the different types of connective tissues and systems, and the role of TGF-beta in development and physiology of soft tissues. This new set of data explains, at least in part, why many of these disorders are interconnected, though the primary pathophysiological events, such as gene mutations, may be different for each disorder.
  • Digital
    J. Robin Harris, editor.
    Springer2012
    Introduction and technical survey: Protein aggregation and fibrillogenesis -- Fibril formation by short synthetic peptides -- In vitrooligomerization and fibrillogenesis of amyloid-beta peptides -- Tau fibrillogenesis -- Prion protein aggregation and fibrillogenesisin vitro -- Alpha-synuclein aggregation and modulating factors -- Pathological self-aggregation of [beta](2)-microglobulin: A challenge for protein biophysics -- Islet amyloid polypeptide: Aggregation and fibrillogenesisin vitroand its inhibition -- Mechanisms of transthyretin aggregation and toxicity -- Fibrillogenesis of huntingtin and other glutamine containing proteins -- Aggregation and fibrillogenesis of proteins not associated with disease: a few case studies -- Experimental inhibition of peptide fibrillogenesis by synthetic peptides, carbohydrates and drugs -- Experimental inhibition of fibrillogenesis and neurotoxicity by amyloid-beta (abeta) and other disease-related peptides/proteins by plant extracts and herbal compounds -- Alzheimer's disease -- Modeling the polyglutamine aggregation pathway in Huntington's disease: from basic studies to clinical applications -- Parkinson's disease -- Human prion diseases: From kuru to variant Creutzfeldt-Jakob disease -- Animal prion diseases -- [beta](2)-Microglobulin amyloidosis -- Systemic AA amyloidosis -- Familial amyloidotic polyneuropathy and transthyretin -- The challenge of systemic immunoglobulin light-chain amyloidosis (AL).
  • Digital
    Rosa Margesin ... [et. al.], editors.
    Springer2008
  • Digital
    Jerome Goddard.
    CRCnetBASE2013
    "Increasing problems of emerging and re-emerging infectious diseases, brought about, at least in part, by vectors fueled by increased worldwide travel and commerce, make this a highly timely book for anyone in the public practice of medical and veterinary entomology, including entomologists, public health officials, and pest control technicians and managers. Employing a reader-friendly style with bulleted texts, scenarios, and case history boxes, it targets the major vectors and pests of medical and public health importance, addresses regulatory and academic medical entomology, and discusses disease vector control with worldwide application"--Provided by publisher.
  • Digital
    Stefanie Duttler.
    One of the most critical times in the life of a protein is during its biogenesis at the ribosome. A nascent polypeptide cannot achieve its final fold while still bound to the ribosome, and is at risk of being accessed by the cellular quality control machinery. However, the extent to which cotranslational ubiquitination and degradation occur remains under debate. Conflicting reports exist, ranging from 40% of nascent chains being subject to cotranslational degradation to claims that nascent polypeptides are, on the contrary, protected from degradation. Here, we developed a direct and quantitative method to determine the extent of cotranslational ubiquitination using ribosome isolation coupled to ubiquitin-affinity purification. We find that cotranslational ubiquitination occurs at low levels, and that at least a fraction of ubiquitinated nascent chains is targeted to the proteasome for degradation. We determined which proteins are susceptible to cotranslational ubiquitination and find that intrinsic sequence features determine the cotranslational ubiquitination of a specific subset of proteins. These proteins are more aggregation-prone, highly expressed and longer than 400 amino acids. Short proteins seem to be protected from cotranslational ubiquitination. One such mechanism could be the cotranslational formation of folded structures, which lead us to disrupt cotranslational folding by deleting chaperones or through drugs such as azetidine-2-carboxylic acid (AZC). Both lead to an increase of cotranslational ubiquitination as observed by pulse-labeling as well as microarray analysis. Ribosome-associated chaperones and cotranslational folding seem to have evolved to prevent a high degree of nascent chain degradation/ubiquitination. Similarly to ribosome-associated chaperones, the ubiquitin-proteasome-system may also be able to access nascent protein chains, but rather target them for degradation. We therefore determined which parts of the UPS mediate cotranslational ubiquitination. A clear E2-E3 relationship could however not be established, possibly due to redundancy in the cellular ubiquitin ligase network. Finally, we find that disruption of mRNA quality control components also leads to enhanced ubiquitination of nascent chains, suggesting that cotranslational quality control serves to avoid the production of erroneous proteins and protect the cell from resulting toxicity.
  • Digital
    edited by Anne Charmantier, Dany Garant, Loeske E.B. Kruuk.
    OSO2014
    1. The study of quantitative genetics in wild populations -- 2. Four decades of estimating heritabilities in wild vertebrate populations -- 3. Quantitative genetic approaches to understanding sexual selection and mating system evolution in the wild -- 4. Individual behaviour : behavioural ecology meets quantitative genetics -- 5. The quantitative genetics of senescence in wild animals -- 6. The effects of others' genes : maternal and other indirect genetic effects -- 7. Dominance genetic variance and inbreeding in natural populations -- 8. Cross-pollination of plants and animals : wild quantitative genetics and plant evolutionary genetics -- 9. Quantitative genetics of wild populations of arthropods -- 10. Case study : quantitative genetics and sexual selection of weaponry in a wild ungulate -- 11. Epigenetic processes and genetic architecture in character origination and evolution -- 12. Evolutionary potential and constraints in wild populations -- 13. Molecular quantitative genetics -- 14. Bayesian approaches to the quantitative genetic analysis of natural populations -- 15. Evolutionary dynamics in response to climate change.
  • Digital
    edited by Adriana Fontes, Beate Saegesser Santos.
    Springer Protocols2014
  • Digital
    Samantha J. Richardson, Vivian Cody [editors].
    Springer2009
  • Digital
    Manuel Eduardo Lopez, Jr.
    Niemann-Pick disease type C (NPC) is a rare metabolic lysosomal storage disorder (LSD) marked by accumulation of large quantities of cholesterol, lipids and other metabolites in cells. Though the disorder has been extensively explored using various genetic animal models, an understanding of the molecular and cellular pathology of the disease remains limited. A cell-type-specific and regulable rescue mouse model of NPC disease was engineered in order to identify the therapeutically relevant cell type and ascertain the effect of inflammation on disease progression. With the current information presented in this dissertation, a probable road map of NPC disease pathology has been drawn. The road map for NPC may also be applicable to, or act as a template for, other lysosomal storage diseases and neurodegenerative disorders with similar pathologies.
  • Digital
    Jaclyn Geok Yueen Lim.
    Adult stem cells are undifferentiated cells that are capable of both self-renewal and differentiation into a variety of specialized cells. Adult stem cell lineages have been identified in several organs including skin, blood, breast, intestine, bladder, skeletal muscle, prostate, and the testes. The changes in homeostatic conditions in these organs caused by tissue turnover or injury rely heavily on the pool of adult stem cells for cell replenishment. Therefore, the activity of adult stem cells must be tightly controlled, and many of these regulations are orchestrated by the stem cell niche, the local microenvironment in which stem cells reside. The fast generation cycle and the genetic tractability of fruit flies make the Drosophila testis stem cell niche an ideal system for the study of adult stem cell regulation. The Drosophila testis maintains two types of stem cells: germline stem cells (GSCs) which give rise to sperm, and cyst stem cells (CySCs) which differentiate into cyst cells that encapsulate germ cells. The somatic cyst cell lineage has been implicated to be required at several stages of spermatogenesis and play pivotal roles in germline proliferation, survival, and differentiation. This dissertation focuses on understanding the role of the cyst cell lineage in GSC maintenance and investigating the mechanisms by which cyst cells direct early germ cell differentiation. Previously, it has been proposed that CySCs are the source of instructive self-renewal cues for GSCs. In contrast to this model, I showed that early germ cells with GSC characteristics can be maintained in the absence of CySCs and cyst cells. These germ cells failed to enter the transit-amplifying program, which is regarded as the first step of differentiation in many adult stem cell lineages. My observations suggest that cyst cells provide a pro-differentiation environment for GSCs, and that this mechanism(s) may be repressed in CySCs which indirectly allow for GSC self-renewal. Encapsulation of germ cells by cyst cells is one of the differentiation-promoting mechanisms imposed by the soma on the germline, and I have uncovered that this process requires activation of the EGFR-Ras-MEK-MAPK pathway in differentiated cyst cells. Furthermore, I also showed that repression of EGFR activation in CySCs is important in maintaining the population of GSCs and CySCs at the niche, as premature activation of the pathway resulted in displacement of GSCs from the hub by somatic cells. Preliminary studies revealed a STAT target gene, Socs36E as a negative regulator of the EGFR pathway in CySCs to prevent out-competition of GSCs by somatic cells. To understand how the somatic cyst cells germline differentiation, I performed two genetic screens: an RNAi screen of genes that caused premature germ cell differentiation when misexpressed in the soma, and a misexpression screen of genes predicted to be cell-surface and secreted proteins. Three promising candidates were identified through these screens: two ribosomal subunits, Rpl13A and RpS10a; and a septate junction component, Neurexin IV. The two ribosomal proteins may be involved in the soma to promote germ cell encapsulation. Neurexin IV however, operates non-cell autonomously in cyst cells to regulate germ cell differentiation into spermatocytes. Together, the results of this dissertation emphasize the importance and complexity of the interaction between adult stem cells and their microenvironment in maintaining tissue homeostasis.
  • Digital
    Daniel Richard Calnan.
    The FoxO family of transcription factors plays an important role in longevity and tumor suppression by regulating the expression of a wide range of target genes. FoxO3 has recently been found to be associated with extreme longevity in humans and to regulate the homeostasis of adult stem cell pools in mammals, which may contribute to longevity. The activity of FoxO3 is controlled by a variety of post-translational modifications that have been proposed to form a 'code' affecting FoxO3 subcellular localization, DNA binding ability, protein-protein interactions and protein stability. Lysine methylation is a key post-translational modification on histones that regulate chromatin accessibility and is a key part of the 'histone code'. However, whether lysine methylation plays a role in modulating FoxO3 activity has never been examined. I found that the methyltransferase Set9 directly methylates FoxO3 in vitro and in cells. Using a combination of tandem mass spectrometry and methyl-specific antibodies, I find that Set9 methylates FoxO3 at a single residue, lysine 271, a site previously known to be deacetylated by Sirt1. Methylation of FoxO3 by Set9 decreases FoxO3 protein stability, while slightly increasing FoxO3 transcriptional activity. The modulation of FoxO3 stability and activity by methylation may be critical for fine-tuning cellular responses to stress stimuli, which may in turn affect FoxO3's ability to promote tumor suppression and longevity. Post-translational modifications control many aspects of FoxO3 activity, including protein stability, subcellular localization and binding partner association. To analyze whether FoxO3 functions primarily alone, or in a complex with other factors, I used size exclusion chromatography to assess the size of the potential FoxO3 protein complexes in cellular extracts. I found that FoxO3 is present in fractions with a relative molecular weight larger ranging from 250 to 700 kDa. Interestingly, the cytoplasmic fraction of FoxO3 appears to be in a larger complex than the nuclear fraction, suggesting that FoxO3 is present in more than one protein complex in cells. To identify novel binding partners of FoxO3 that could be present in these large molecular-weight protein complexes, I conducted a tandem affinity purification (TAP) of dual tagged FoxO3 in HeLa S3 cells followed by liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) of the elution from the immunoprecipitation. I identified over 1,000 potential FoxO3 binding partners that were not present in the control immunoprecipitation. These candidate binding partners included protein kinases (e.g. mTOR, MAPKs), other tumor suppressors (e.g. p65, p130) and oncogenes (e.g.Myb), as well as proteins that contain a methyl lysine (e.g. WDR17, PHF3) and acetyl lysine (e.g. BAZ2B, BRD1) binding domains. Taken together, these results suggest that FoxO3 functions in large protein complexes that could affect FoxO3 activity. The formation of FoxO3-containing complexes could be triggered by FoxO3 post-translational modifications. By increasing our understanding of the regulation of FoxO3, as well identifying possible interacting proteins, we further our knowledge of the pathways important for both longevity and age related diseases, including cancer.
  • Digital
    NAP2007
  • Digital
    Peggie Cheung.
    Epigenetics is the study of heritable changes in gene expression that occur independent of changes in the primary DNA sequence. Chromatin structure defines the state in which genetic information is organized in the cell. The organization of this structure greatly influences the abilities of genes to be activated or silenced. In eukaryotic cells, 146 base pairs of DNA is wrapped around the histone octamer (two H2A/H2B dimers and one H3/H4 tetramer) forming the nucleosomes, the basic unit of chromatin. The nucleosome cores are connected by linker DNA sequences to further package into higher-order chromatin structures. In addition to the core histones, each histone contains an unstructured N-terminal tail. The histone tails are the sites of most of the post-translational modifications (PTMs), such as acetylation, methylation and phosphorylation. These modifications regulate the structure and function of chromatin through two general mechanisms. In the first model, histone modifications may play a direct role in altering chromatin structure. For example, histone acetylation neutralizes the positive charge of lysine residues and thus, affecting the interactions of the histones with DNA, transcription factors and other nucleosomes. Secondly, histone modifications can indirectly affect chromatin functions by serving as a binding platform for modular proteins and complexes. For instance, the methylation of histone H3 at lysine 9 is recognized specifically by the chromatin organization modifier (Chromo) domain of heterochromatin protein 1 (HP1), which contributes to the induction and the propagation of heterochromatin structure. Ten years ago, Strahl and Allis proposed a general idea of "histone code" hypothesis, which states that histone modifications, distinct or in combination, to form a "code" to influence chromatin structure and lead to varied transcriptional outputs. In recent years, many chromatin regulators were identified, such as the proteins that "write" or "erase" or "read" the modifications. Some chromatin regulators are expressed in a tissue-specific manner and play important roles in physiology and disease pathogenesis. For instance, the H3K27 histone methyltransferase EZH2 is overexpressed in tumors such as prostate, breast, colon, skin and lung cancer. Disruption of normal patterns of covalent histone modifications is another hallmark of cancer. One of the most characterized examples is the global reduction of the trimethylation of H4K20 and acetylation of H4K16, along with hypomethylation, at repeat sequences in many tumors. Since post-translational modifications have been shown to be important for many biological processes such as gene expression, DNA damage and repair and apoptosis, disruption of these processes has been linked to carcinogenesis and other disease pathogenesis. The discovery of reversible mutations in the epigenetic machinery makes post-translational modifications as one of the most promising and expanding fields in the current biomedical research. Methylation does not neutralize the charge of the modified residue nor does addition of methyl groups add considerable bulk, this mark is believed to create a distinct molecular architecture on histones that is recognized by specialized binding domains present within chromatin-regulatory proteins. The proteins and domains that recognize histone modifications, named "effectors" or "readers", are thought to define the functional consequences of lysine methylation by transducing molecular events at chromatin into biological outcomes. Mutations in these "readers" proteins have been shown to link to many disease pathogenesis. However, relatively few effector domains have been identified in comparison to the number of modifications present on histones and non-histone proteins. Here we developed a human epigenome peptide microarray platform (HEMP) for high-throughput discovery of chromatin effectors. We probed this platform with modification-specific antibodies and known chromatin effector domains to test the integrity of the peptides on the slides. We also screened a library of Royal Domain family members and identified three effector proteins with novel modified-histone binding activity. Hence, the development of the HEMP facilitates the identification of effector proteins and understanding of chromatin signaling networks. Multiple Myeloma (MM) is a malignancy of bone marrow plasma cells that frequently results in bone marrow destruction, bone marrow failure and death. 15% of patients with multiple myeloma is diagnosed with an immunoglobin gene, t(4; 14), translocation. MM patients carrying the t(4; 14) translocation is associated with the overexpression of WHSC1/MMSET/NSD2. NSD2 is a protein lysine methylatransferase in the nuclear receptor binding SET domain protein family. However, the molecular mechanism by which NSD2 contributes to myeloma pathogenesis is not known. Here we show that the dimethylation of histone H3 at lysine 36 (H3K36) is the principal physiological activity of NSD2. In mammalian cells, H3K36me2 normally maps to gene bodies. In t(4; 14)+ myeloma cells, overexpression of NSD2 disrupts the physiologic genomic organization of H3K36me2 which is found being dispersed throughout the genome. NSD2 expression is linked to transcription activation and H3K36me2 location at gene bodies positively correlates with transcription levels. In Myeloma cells, NSD2-mediated localized elevation of H3K36me2 induces transcription at normally inert cancer-associated genes. Catalytic activity of NSD2 confers tumor formation in xenograft model and promotes oncogenic transformation of primary cells by regulating transcriptional programs that favor oncogenesis. The BAH domain is an evolutionarily conserved chromatin-associated motif. Utilizing the HEMP, we screened several BAH domains from yeast and human for binding activity. We found that the BAH domain of human ORC1 specifically bind to H4K20me2 peptides. Structural studies show that BAH domain has an aromatic dimethyl-lysine-binding cage that interacts with the bound peptide. ORC1 is dispensable for ORC complex assembly but is necessary for loading of the complex into chromatin. The ability of ORC1 BAH domain binding to H4K20me2 is required for the efficient stabilization of ORC complex at chromatin. H4K20me2 is enriched at replication origins. Abrogation in ORC1 and H4K20me2 interactions impairs cell-cycle progression. Mutations in ORC1 BAH domain have been implicated in aetiology of Meier-Gorlin syndrome (MGS), a form of primordial dwarfism. In a zebrafish model, orc1 morphants display an MGS-like dwarfism phenotype, which can be rescued by wild type Orc1 but not ORC1 binding mutants. Zebrafish depleted with H4K20me2 also displays the MGS-like phenotype. Together, our findings reveal a new function for histone methylation signaling at chromatin in the regulation of DNA replication and organismal growth. KDM2A is the first jumonjiC domain-containing demethylase identified. We solved the co-crystal structure of KDM2A and its substrate, H3K36me2. We found that KDM2A demethylation activity is required to maintain genomic stability. We also show that KDM2A is a tumor suppressor and its demethylation activity is required for suppressing cellular transformation.
  • Digital
    Kelly Elizabeth McCann.
    Efficient DNA double-strand break (DSB) repair is essential for maintaining the stability of the genome. A single long-lived DSB can cause cell lethality (Bennett et al., 1996). Humans with defects in DSB repair are sensitive to DNA damaging agents and are predisposed to developing cancers, as exemplified by such diseases as Nijmegan breakage syndrome, Ataxia telangiectasia, and breast cancer susceptibility in women with mutations in the BRCA1 and BRCA2 genes (Duker, 2002). Repair of DNA damage requires activation of cell cycle checkpoint controls, recruitment of repair proteins to DNA lesions, and transcriptional activation of relevant genes. As shown by our data, deletion of particular histone modification genes produces sensitivity to ionizing radiation in Saccharomyces cerevisiae, suggesting a role for chromatin modification enzymes in the repair process as well. Because damage recognition and repair of lesions are both influenced by chromatin structure, we began by studying the role of histone acetylation in the DNA damage response. Acetylation of the N-terminal tails of histone H4 opens the chromatin to allow repair enzymes to access broken DNA. Through a screen of the yeast deletion pool, we found that deletion of BRE1 and DOT1 genes causes sensitivity to ionizing radiation. Ubiquitination of H2B on lysine 123 (H2B-K123) by ubiquitin ligase Bre1 is necessary for methylation of H3 on lysine 79 (H3-K79) by Dot1. Through the histone modifications they catalyze, these proteins are involved in many aspects of the DNA repair response, as outlined in Sections C, D, and E. Our studies focused on homologous recombination repair defects, genome-wide expression patterns in BRE1 and DOT1 deletion mutants, an analysis of the data regarding proteins purported to bind to methylated H3-K79, and optimization of a protein purification strategy to find Dot1 binding partners. Our yeast deletion pool screen also predicted a role for N-terminal acetyltransferase complex NatB in DNA double-strand break repair. In Section F, we build a case for acetylation of DNA end-binding protein Mre11.
  • Digital
    Brian A. Baldo.
    Springer2016
    1: Approved Biologics Used For Therapy and their Adverse Effects -- 2: Monoclonal Antibodies: Introduction -- 3: Monoclonal Antibodies Approved for Cancer Therapy -- 4: Other Approved Therapeutic Monoclonal Antibodies -- 5: Cytokines -- 6: Fusion Proteins -- 7: Peptide Hormones -- 8: Glycoprotein Hormones -- 9: Enzymes Approved for Therapy -- 10: Blood Coagulation -- 11: Vaccines -- 12: Botulinum Neurotoxins -- 13: Biosimilars.
  • Digital
    Julie Rebecca Perlin.
    The nervous system connects cells throughout the body to coordinate actions and transmit signals. Critical to the nervous system are the neurons that extend axons to their targets and the glial cells that interact with these axons. Oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system wrap axons to make the myelin sheath. Myelin is critical for enhancing the speed of action potentials as well as providing support to axons. Myelin was a critical adaptation that has allowed vertebrates to increase in size, precision of movement, and complexity. Insults to myelin cause devastating diseases, and a better understanding of the normal development of myelinating glia is necessary for improving treatment of human neuropathies. In this dissertation I investigate both well-known and novel signaling pathways and their roles in Schwann cell migration and myelination in zebrafish peripheral nerves. Before making myelin, Schwann cells must migrate along and cover the surface of a bundle of axons. Here, I demonstrate that Neuregulin 1 type III (Nrg 1 type III) is required in neurons to signal through ErbB receptors in Schwann cells for Schwann cell migration along the posterior lateral line nerve, a mechanosensory nerve. Further, ectopic expression of this signal in all neurons is sufficient to attract peripheral Schwann cells into the spinal cord. There appears to be distinct regulation of Schwann cell migration in different nerves of the peripheral nervous system, as migration of Schwann cells in motor nerves requires ErbB receptors but not the Nrg 1 type III ligand. Nrg1 type III does, however, control myelination in both sensory and motor nerves. Schwann cell migration is not only important to properly localize Schwann cells, but also to localize the lateral line nerve itself, which begins in the epidermis but then transitions across a basement membrane to the subepidermal space. As they migrate, Schwann cells degrade the basement membrane beneath the skin, which allows the nerve to transition out of the epidermis, and then rebuild the basement membrane after the nerve has been repositioned and protected from the disorganization that otherwise would take place if it remained in the epidermis. Finally, through analysis of a mutation that was found in a forward genetic screen for genes essential in myelination, I also identify a novel regulator of Schwann cell myelination. Together this work elucidates new roles of known genes in Schwann cell and nerve development and also identifies a novel gene required for peripheral myelination.
  • Digital
    Sara Elaine Brownell.
    This thesis explores the use of small heat shock proteins as anti-inflammatory therapeutics in the context of neurological diseases, specifically multiple sclerosis (MS) and stroke. The family of small heat shock proteins (sHSPs) has been extensively studied as intracellular molecular chaperones. However, recent studies looking at the role of sHSPs in neurological diseases have demonstrated a near universal upregulation of certain sHSPs in damaged and diseased brains. Initially, it was thought that sHSPs are pathological in these disease states, but transgenic overexpression and exogenous administration of sHSPs in various experimental disease paradigms have shown just the contrary -- that sHSPs are protective, not pathological. In this thesis, I have found that members of the family of sHSPs are protective and therapeutic in mouse models of multiple sclerosis and stroke, experimental autoimmune encephalomyelitis (EAE) and middle cerebral artery occlusion (MCAO), respectively. Alpha B crystallin (cryab), a member of the sHSP family, is elevated in stroke and deficiency of cryab leads to worse disease outcome, illustrating the protective role of alpha B crystallin. Exogenous administration of small heat shock proteins, including alpha B crystallin, decreases disease severity by modulating the immune system. This leads to the conclusion that sHSPs are endogenous anti-inflammatory and neuroprotectant molecules produced after neurological disease, whose beneficial properties can be augmented when administered therapeutically.
  • Digital
    Eckart Eich.
    Springer2008
  • Digital
    Alexander Gray Vaughan.
    This thesis encompasses three projects at the intersection of genetics, behavior, and neurobiology in the fruitfly, Drosophila melanogaster. The major work presented is an investigation of the afferent auditory system in D. melanogaster. The afferent auditory system of D. melanogaster arises from the Johnston's Organ in the second antennal segment, from which mechanosensory neurons project to a protocerebral region known as the Antennomechanosensory and Motor Complex (AMMC). The antennal mechanosensory system in Drosophila is used in multiple contexts, including vestibular mechanosensation, wind sensitivity, and courtship hearing. During courtship, male flies present a stereotypic pulse song as well as a hum-like sine-song to female flies; these stimuli are species-specific and critical to female receptivity. Using a large enhancer-Gal4 collection, I identify 12 candidate cell types within the AMMC, divided into 7 types of projection neurons as well as 5 types of local AMMC interneurons. I tested each of these cell types for its effect on courtship hearing by testing the effect of neuronal silencing on a) female receptivity, and b) a male locomotor response (Song-Induced Locomotion). These tests reveal that the activity of one class of projection neuron (aPN1), and one class of local interneuron (aLN(al)) are critical to courtship hearing in both male and female flies. Other cell types appear to be dispensable for courtship hearing, and may play a role in non-courtship related mechanosensation. To help confirm that these phenotypes are not specific to neuronal silencing, I also hyperactivated each cell type using the temperature-sensitive dTrpA1 reagent; these results confirm that aPN1 and aLN(al) alone are necessary for courtship hearing. Overall this work identifies a set of parallel pathways from the AMMC leading to the ventrolateral protocerebrum (VLPR), but reveal that only one of these pathways is necessary for courtship hearing. The structure of this circuit is analogous to the multi-lineage projection identified in D. melanogaster olfaction, in which a parallel pathways share a common projection but carry independent information. In addition to this work, I also discuss an investigation of the role of abnormal-chemosensory jump 6 (acj6) on escape behaviors, as well as an investigation of the expression of doublesex (dsx) in the nervous system.
  • Print
    John S. Wilkins.
    In this comprehensive work, John S. Wilkins traces the history of the idea of "species" from antiquity to today, providing a new perspective on the relationship between philosophical and biological approaches.--[Book cover].
  • Digital/Print
    Digital : SpringerLink2005-
  • Digital
    Kerri A. Spilker.
    Specification and assembly of synapses is a highly coordinated and regulated process. Knowledge of the position and connectivity of all C. elegans neurons makes it a highly useful organism for studying the underlying mechanisms that control synapse formation. Using cell-specific promoters and fluorescently-labeled synaptic vesicle proteins, we are able to monitor synapse formation in subsets of C. elegans neurons. Close observation of synapse formation in a single posterior motorneuron (DA9) led to the identification of a mutation in the alternative splicing regulator mbl-1 that changes the synaptic pattern. The cholinergic motorneuron DA9 is required for backwards locomotion and forms ~25 synapses onto both inhibitory neurons and body wall muscles in the dorsal nerve cord (DNC) of the worm. We found that the 10 most distal synapses of DA9 fail to form in mbl-1 mutants, visualized with the synaptic vesicle-associated protein RAB-3 and the active zone proteins SYD-2/liprin-[Alpha] and UNC-10/Rim. In addition, some RAB-3 mis-localizes to the dendrite of DA9 and animals have a backwards locomotion defect consistent with a loss of synapses onto dorsal body wall muscles. mbl-1 is a member of the conserved MBNL (Muscleblind like) family of CCCH zinc-finger RNA binding proteins that regulate alternative splicing of target genes by directly binding to target mRNA. In the human disease myotonic dystrophy type 1 (DM1), a progressive muscular dystrophy, sequestration of MBNL proteins in nuclear foci leads to altered splicing of downstream genes. Mis-splicing of several genes is responsible for the muscular and cardiac symptoms present in individuals with DM1. Most work on the MBNL proteins has focused on their role in muscle morphogenesis and maintenance. However, C. elegans mbl-1 is expressed in a subset of motorneurons including DA9 and is required cell autonomously in these neurons to regulate proper synapse formation. Post-synaptic and muscle markers were unaffected in mbl-1 mutant animals. Thus, our work demonstrates that mbl-1 also functions in neurons to regulate synapse formation. In a separate set of experiments, we identified a new mutation in the coding region of the touch cell-specific beta-tubulin, mec-7(wy116) that causes a defect in synapse formation in the mechanosensory neuron PLM. Previous studies have shown that mec-7 is expressed exclusively in the six touch neurons of C. elegans and is required for sensing light touch. Our mec-7 mutation leads to a loss of synaptic vesicle accumulation at PLM synaptic sites in the ventral nerve cord and synaptic vesicles are visible at ectopic locations along the lateral axon of PLM. Localization of the synaptic proteins VAMP and GIT-1 is also defective in our mutant, but neuronal morphology is wild-type. mec-7(wy116) is mildly Mec, but other alleles of mec-7 (e1506, e1527) do not phenocopy the synaptic vesicle localization defect. mec-7(wy116) is a missense mutation that alters a highly conserved Thr at position 409 to Ile. Crystal structures of tubulin indicate that this residue is on the face of tubulin that interacts with kinesin motor. Because we see synaptic vesicles along the lateral axon of PLM, we believe that kinesin-mediated vesicle transport is less efficient in mec-7(wy116) mutants.
  • Digital
    edited by Huimin Zhao.
    ScienceDirect2013
    Synthetic Biology provides a framework to examine key enabling components in the emerging area of synthetic biology. Chapters contributed by leaders in the field address tools and methodologies developed for engineering biological systems at many levels, including molecular, pathway, network, whole cell, and multi-cell levels. The book highlights exciting practical applications of synthetic biology such as microbial production of biofuels and drugs, artificial cells, synthetic viruses, and artificial photosynthesis. The roles of computers and computational design are discussed, as well as future prospects in the field, including cell-free synthetic biology and engineering synthetic ecosystems. Synthetic biology is the design and construction of new biological entities, such as enzymes, genetic circuits, and cells, or the redesign of existing biological systems. It builds on the advances in molecular, cell, and systems biology and seeks to transform biology in the same way that synthesis transformed chemistry and integrated circuit design transformed computing. The element that distinguishes synthetic biology from traditional molecular and cellular biology is the focus on the design and construction of core components that can be modeled, understood, and tuned to meet specific performance criteria and the assembly of these smaller parts and devices into larger integrated systems that solve specific biotechnology problems. Includes contributions from leaders in the field presents examples of ambitious synthetic biology efforts including creation of artificial cells from scratch, cell-free synthesis of chemicals, fuels, and proteins, engineering of artificial photosynthesis for biofuels production, and creation of unnatural living organisms. Describes the latest state-of-the-art tools developed for low-cost synthesis of ever-increasing sizes of DNA and efficient modification of proteins, pathways, and genomesHighlights key technologies for analyzing biological systems at the genomic, proteomic, and metabolomic levels which are especially valuable in pathway, whole cell, and multi-cell applications. Details mathematical modeling tools and computational tools which can dramatically increase the speed of the design process as well as reduce the cost of development.
  • Digital
    Michael G. Katze, editor.
    Springer2013
    First, systems biology is an inter-disciplinary approach, requiring the combined talents of biologists, mathematicians, and computer scientists. Second, systems biology is holistic, with the goal of obtaining a comprehensive understanding of the workings of biological systems. This is achieved through the acquisition of massive amounts of data by high-throughput technologies-oligonucleotide microarrays, mass spectrometry, and next-generation sequencing-and the analysis of this data through sophisticated mathematical algorithms.
  • Digital
    Choi, Sangdun.
    Springerv. 1-, 2010-
  • Digital
    An online journal and ebook service of the Thieme Publishing Group. The ebook package is also called Thieme Clinical Collections.
  • Digital
    Bronner, Felix; Farach-Carson, Mary C.
    Springerv. 2-, 2005-
  • Digital
    edited by Alessandro Minelli, Thomas Pradeu.
    OSO2014
    Is it possible to explain and predict the development of living things? What is development? Answers to these innocuous questions are far from straightforward. To date, no systematic, targeted effort has been made to construct a unifying theory of development. This text offers a unique exploration of the foundations of ontogeny by asking how the development of living things should be understood. It explores the key concepts of developmental biology, asks whether general principles of development can be discovered, and examines the role of models and theories. This book analyses a wealth of approaches to concepts, models and theories of development, such as gene regulatory networks, accounts based on systems biology and on physics of soft matter, the different articulations of evolution and development, symbiont-induced development, as well as the widely discussed concepts of positional information and morphogenetic field, the idea of a 'programme' of development and its critiques, and the long-standing opposition between preformationist and epigenetic conceptions of development.
  • Digital
    editor, Gian Paolo Rossini.
    CRCnetBASEv.1 (2014)
    CRCnetBASEv.2 (2014)
    Structured account of the existing knowledge of toxic algae, the chemistry of the toxins they produce, the effects these substances exert in humans and wildlife, as well as the strategies envisaged to protect public health and the environment. Covers recent advances in the understanding of the biology of toxin producers and the factors involved in the appearance and dynamics of harmful algae blooms, the factors affecting toxin production, the synthesis of toxins both in natural producers and by chemical means in a lab, and the toxin groups posing continuing and novel. Studies effects toxic microalgae and their poisonous products exert on living systems and how they may affect human activities.
  • Digital
    Hugh Cartwright ; chapter 10, Evolvable developmental systems, contributed by Nawwaf Kharma.
    CRCnetBASE2008
  • Digital
    Alan Hunter Shain.
    Pancreatic ductal adenocarcinoma, subsequently referred to as pancreatic cancer, is one of the most deadly cancers with a five-year survival of only 5%. Typical treatment regimens include surgery and chemotherapy while targeted therapies are lacking. A better understanding of the underlying cancer biology may yield novel therapeutic targets. The field of genomics has transformed our ability to study cancer. Over the past two decades, microarray and sequencing based innovations have enabled biology to be carried out at the --omic scale (discussed further in Chapter 1). This dissertation employs --omic level analysis to query the differences between the pancreatic cancer genome and the normal human genome. First, high throughput structural characterizations were performed in order to annotate the mutated, rearranged, deleted, and amplified genes across seventy pancreatic cancers. These assays identified hundreds of candidate cancer genes. Among these candidates, SMURF1 was validated to be an oncogene (Chapter 2). Furthermore, various subunits of the SWI/SNF chromatin remodeling complex were validated to be tumor suppressor genes (Chapter 3). While SMURF1 and SWI/SNF were validated individually, the other candidates from structural studies were evaluated in parallel shRNA competive growth screen. From this, we characterize nine genes further -- some previously known to play a role in cancer and some novel (Chapter 4). The sum total of all of this work is a much deeper understanding of the biology of pancreatic cancer, yielding many novel therapeutic targets and hopefully allowing scientists to gain a foothold in the fight against this disease.
  • Digital
    H.G. Stratmann.
    Springer2016
  • Digital
    Boris Bogdan, Ralph Villiger.
    Springer2008
  • Digital/Print
    Michael G. Rossmann, Venigalla B. Rao, editors.
    Digital : Springer2012
    Print2012
    Viruses: sophisticated biological machines / M.G. Rossmann and V.B. Rao -- F(1)-ATPase: A prototypical rotary molecular motor / K. Kinosita, Jr. -- Principles of virus structural organization / B.V. Prasad and M.F. Schmid -- Reconstructing virus structures from nanometer to near-atomic resolutions with cryo-electron microscopy and tomography / J. Chang ... [et al.] -- Contractile tail machines of bacteriophages / P.G. Leiman and M.M. Shneider -- Long noncontractile tail machines of bacteriophages / A.R. Davidson ... [et al.] -- Short noncontractile tail machines: adsorption and DNA delivery by podoviruses / S.R. Casjens and I.J. Molineux -- Infection of cells by alphaviruses / D.T. Brown and R. Hernandez -- Influenza virus entry / M. Luo -- Molecular mechanisms of HIV entry / C.B. Wilen, J.C. Tilton and R.W. Doms -- Bunyavirus: structure and replication / T.S. Guu, W. Zheng and Y.J. Tao -- Viral polymerases / K.H. Choi -- Chaperonin-mediated folding of viral proteins / Z.L. Hildenbrand and R.A. Bernal -- Building the machines: scaffolding protein functions during bacteriophage morphogenesis / P.E. Prevelige and B.A. Fane -- Bacteriophage HK97 capsid assembly and maturation / R.W. Hendrix and J.E. Johnson -- Lipid-containing viruses: Bacteriophage PRD1 assembly / S.J. Butcher, V. Manole and N.J. Karhu -- Assembly of large icosahedral double-stranded RNA viruses / M.M. Poranen and D.H. Bamford -- The papillomavirus virion: a machine built to hide molecular Achilles' heels / C.B. Buck and B.L. Trus -- Procapsid assembly, maturation, nuclear exit: dynamic steps in the production of infectious herpesvirions / G. Cardone ... [et al.] -- Assembly and architecture of HIV / B.K. Ganser-Pornillos, M. Yeager and O. Pornillos -- Condensed genome structure / L.W. Black and J.A. Thomas -- The bacteriophage DNA packaging machine / M. Feiss and V.B. Rao -- The dsDNA packaging motor in Bacteriophage o29 / M.C. Morais -- Single-molecule studies of viral DNA packaging / Y.R. Chemla and D.E. Smith -- Genome gating in tailed bacteriophage capsids / P. Tavares, S. Zinn-Justin and E.V. Orlova -- Packaging in dsRNA Viruses / L. Mindich -- Mechanism of RNA packaging motor / E.J. Mancini and R. Tuma -- Helical viruses / G. Stubbs and A. Kendall.
  • Digital
    Li Ling.
    The mammalian nervous system consists of billions of neurons arranged into complicated networks (neuronal circuits) that mediate all aspects of brain function and behavior. A fundamental goal of neuroscience is to describe the structure of neural circuits at the level of single cells and to understand how this structure enables information acquisition, processing, storage, and ultimately the control of behavior. Over the past hundred years, the cumulative efforts of many individuals have led to the development of a wide array of neuronal labeling tools. First, in this thesis, with the ultimate goal of further expanding genetically coded labeling tools to visualize the presynaptic distribution in single neurons within the mouse brain in vivo, I developed a new genetic synaptic labeling method and used it to analyze the spatial patterning of synapses in developing and mature cerebellar granule. Second, taking the advantage of the MADM system that allows gene knockout in single cells and simultaneously labeling the cells for morphology characterization, I also utilized MADM to study the function of the Rai1 gene, heterozygosity of which results in Smith-Magenis Syndrome in human.
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