bluuebunny/crossref_metadata_2025_split huggingface dataset:
Vaccination of Animals
Authors: Babiuk Lorne A , Stokka Gerald L , Gaspers James J 
Published: February 2018

Abstract

The practice of vaccination to elicit an immune response has been utilised to reduce the risk of infectious disease for hundreds of years. Regarding the health of livestock, vaccination remains one of the most, if not the most, important management tools for the prevention of infectious diseases. The goal of any vaccine and vaccination protocol is to reduce the risks associated with the development of clinical disease. Various approaches can be employed to improve animal health through vaccination. Owing to the unique management situation faced by different species, each has its own difficulties associated with vaccine delivery and eliciting the proper long‐lived immunologic responses. Understanding these difficulties with vaccine delivery, the pathogens themselves and the specific species immune response to vaccine antigens is critical to further reduce the risks of clinical disease.

Key Concepts

Infectious diseases continue to persist in animal populations and it is critical to understand each individual species from a management standpoint as well as the pathogenesis of the infectious agent in order to illicit the specific immune response required to deliver life‐long protection from clinical disease.

Understanding the passive transfer of immunity from mother to offspring as well its effect on the neonate's ability to produce a proper immune response to vaccine antigens is required.

Anticipating stressful events in an animal's life and applying vaccination protocols before those events take place so that the animal's immune system is effectively able to recognise and combat the antigen(s) is critical to the success of the vaccine and the animal.

Matching economic viability and vaccination principles with vaccination protocols is required to achieve biological control of pathogens.

Understanding various routes of vaccine administration and the specific immune response they illicit is necessary for the success of a vaccine and vaccination protocol.

Understanding the dynamics of pathogen transmission and the concept of herd immunity.

Cooperation among research scientists, veterinarians, owners of the animals and government agencies is critical for the widespread eradication of specific diseases.
Transgenic Animals
Authors: Houdebine Louis M 
Published: February 2018

Abstract

Transgenesis implies that a foreign deoxyribonucleic acid (DNA) fragment is introduced into the genome of a multicellular organism and transmitted to progeny. Transgenesis, therefore, differs from gene transfer into cultured cells (transfection) or into the somatic cells of a patient (gene therapy). The foreign DNA can integrate randomly in host genome leading to gene addition or in a targeted manner making it possible precise endogenous gene inactivation or replacement. Transgenesis allows transferring genes from any source in a single generation. Transgenesis is, therefore, complementary to spontaneous mutations, which take place at each reproduction cycle or which are experimentally induced by mutagenic compounds or irradiation. These conventional approaches must be followed by appropriate selection of animals. Transgenesis has become an essential tool to study gene function especially in the medical and pharmaceutical fields. Improvements of breeding and food are also in course. Recent techniques based on the targeted gene modification make it much easier specific gene knockout and gene replacement in animals. The CRISPR‐Cas9 system is the most currently used system.

Key Concepts

Transgenesis is more precise and more diverse than conventional selection.

Transgenesis and conventional selection are complementary.

Transgenesis is an essential tool to study gene action and control.

Cloning is presently intensively used to generate transgenic farm animals.

Stem cells are currently used for random and targeted gene integration.

Targeted gene integration using double‐strand genomic DNA break provides researchers with exceptionally efficient new tools.

Conventional targeted gene transfer is limited by its low efficiency.

SiRNAs are efficient tools to inhibit gene expression at the mRNA level.

The available tools to generate transgenic animals offer the possibility to develop more relevant biological models and to prepare safer food.

Animal behaviourists must participate in conservation planning to protect the future of biodiversity.
Cleavage and Gastrulation in the Mouse Embryo
Authors: Nahaboo Wallis , Migeotte Isabelle 
Published: February 2018

Abstract

After fertilisation of the oocyte, the mouse zygote divides three times before undergoing compaction, which allows polarisation of the blastomeres, and the first lineage specification between trophectoderm (destined to become placenta) and inner cell mass (ICM). The second lineage specification occurs at the blastocyst stage, when ICM cells become either epiblast (which will give rise to the embryo proper) or primitive endoderm (an extraembryonic lineage). After implantation, the proximal (site of attachment with the uterus)‐distal axis is established, quickly followed by the determination of the anterior–posterior axis. Formation of the three main germ layers, ectoderm, mesoderm and endoderm, then occurs on the posterior side at the primitive streak, site of gastrulation. However, recent advances in mouse embryo live imaging have shown that lineage specification was more flexible than previously thought. It has also become possible to visualise the early stages of human embryo development.

Key Concepts

Early mouse embryo development proceeds through a sequence of lineages specification events.

Similar signalling pathways are reused at different steps of early development.

Positional and mechanical cues play essential roles for cell lineage specification and morphogenesis.

The initial steps, up to and including gastrulation, are quite conserved between all amniotes.

The main differences at later stages reside in the extraembryonic tissues, as mammals have adapted to internal gestation through the development of a placenta.
Human Leucocyte Antigen (
HLA
) System and Human Disorders
Authors: Traherne James A 
Published: February 2018

Abstract

The major histocompatibility complex (MHC) has been studied in depth because it is associated genetically with more human disorders than any other region in the human genome. In addition to the human leucocyte antigen (HLA) genes, the MHC contains a diverse array of multiallelic genes, many of which are involved in modulating the immune response to pathogens. Advanced mapping and sequencing approaches are helping to define more precisely contributions of MHC variants to disease. Class I or class II molecules are confirmed as the primary influence in most studies, attesting to their functional impact on antigenic peptide presentation to lymphocytes. Regulatory polymorphism controlling cell surface expression of HLA molecules has also been associated with disease. However, the precise causal nature of the majority of associated alleles and haplotypes with disease is still not understood.

Key Concepts

The MHC encodes genes essential for immunity in humans, including the HLA molecules.

With the exception of one gene,
HLA‐DRA
, the classical HLA genes are highly variable.

HLA class I and II genes are associated with many diseases, including infectious diseases, cancers and neuropathies but particularly autoimmunity.

Many HLA variants are concurrently associated with both infectious and autoimmune diseases.

The MHC may be considered as a cluster of genes with integrated functions.

A high proportion of MHC genes are involved in immunity.

The MHC contains nonclassical class I and II genes, such as HLA‐E, F and G, and HLA‐DM, DO, respectively.
DNA
Helicase Deficiency Disorders
Authors: Sidorova Julia M , Monnat Jr Raymond J 
Published: February 2018

Abstract

Deoxyribonucleic acid (DNA) helicases use energy derived from ATP (adenosine triphosphate) hydrolysis to separate the complementary strands of DNA. This article focuses on one family of DNA helicases, the human RECQ helicases, and the syndromes that arise in their absence or following loss of function. The five human RECQ helicases share a common, conserved helicase domain, and all five proteins play important roles in cellular DNA metabolism. Loss of function mutations in three family members cause the human cancer predisposition syndromes Bloom syndrome (BS), Werner syndrome (WS) and Rothmund–Thomson syndrome (RTS). This article outlines clinical features of the RECQ helicase deficiency syndromes, and reviews our understanding of the genetics, biochemistry and function of the syndrome‐associated RECQ helicases. We discuss how the loss of RECQ function may promote genetic instability and disease pathogenesis, and how RECQ helicases may serve as predictors of cancer risk and the response to therapy.

Key Concepts

RECQ helicases are found in all Kingdoms of life.

RECQ helicases use the energy of ATP hydrolysis to unwind the two strands of DNA.

RECQ helicases function in important aspects of DNA metabolism including DNA replication and repair, recombination, transcription and telomere maintenance.

Loss of RECQ helicase function is associated with DNA metabolic defects, genetic instability, reduced cell proliferation and cellular senescence or apoptosis.

Three rare, distinct heritable recessive human RECQ helicase deficiency syndromes have been identified. RECQ helicase‐deficient individuals have an elevated risk of cancer and additional developmental or acquired findings.

Altered RECQ helicase function may be common in adult cancer, and may affect both cell viability and the response to therapy.

RECQ‐specific inhibitors may be therapeutically useful in a subset of human cancers.
Telomeres and Telomerase in Ageing and Cancer
Authors: Ouellette Michel M 
Published: February 2018

Abstract

Telomeres are protective structures that cap the ends of linear chromosomes. In humans, they are made of a repetitive DNA (deoxyribonucleic acid) sequence, (TTAGGG)

n

, and associated proteins. Because DNA polymerases are unable to completely replicate the ends of linear chromosomes, telomeres shorten each time cells divide. This gradual shortening of the telomeres limits their cellular lifespan and contributes to the ageing process. During cancer development, this obstacle to immortality is almost always bypassed by the overexpression of telomerase, a specialised reverse transcriptase that functions to add back telomeric repeats to telomeres. In humans, its expression is limited to rare stem cells of renewal tissues, but a notable exception has been its overexpression in the great majority of cancers. Accordingly, telomerase is being developed as both a novel marker for the detection of cancer cells and a novel target for the treatment of cancers. Herein, we discuss the role of telomeres and telomerase in cancer and ageing, with the emphasis on potential future applications in the treatments of cancers and age‐related diseases.

Key Concepts

Telomeres are protective structures that cap the ends of chromosomes.

Human telomeres are made of TTAGGG DNA repeats and associated proteins.

Because of ‘end replication problems’, telomeres shorten each time cells divide, and this shortening limits cellular lifespan and contributes to the ageing process.

Telomerase is a specialised reverse transcriptase that functions to add back telomeric repeats to the ends of telomeres, thereby extending cellular lifespan.

Telomerase expression in humans is limited to rare stem cells of renewal tissues (gastrointestinal track, blood and skin).

Telomerase is almost always aberrantly overexpressed in cancer. This overexpression is detected in 85% of all cancers, irrespective of the tumour type.

Telomerase is being developed as a marker to allow the detection of cancer cells in otherwise telomerase‐negative normal tissues.

Inhibitors of telomerase are being developed to limit tumour growth and reduce the incidence of recurrences following conventional cancer therapy.

Strategies for transient telomerase reactivation are also being developed for the treatment of degenerative diseases and age‐related diseases.
Lissencephaly, Genetics of
Authors: Passemard Sandrine , Chalard François , Verloes Alain , Gressens Pierre 
Published: February 2018

AbstractThe term lissencephaly (literally ‘smooth brain’) covers rare malformations of the brain characterised by a paucity of normal gyri and sulci with absent (agyria) or abnormally wide gyri (pachygyria) associated with an abnormal cortical layering. Different forms of lissencephalies have been described: classical lissencephalies (also called type I) and their variants, and cobblestone lissencephalies (also called type II). Classical lissencephalies include lissencephalies with mutations inLIS1,DCX,ARXorTUBA1genes, isolated lissencephalies without any identified genetic defect, lissencephalies with severe microcephaly (microlissencephaly) and lissencephalies associated with syndromes including multiple malformations. The cobblestone lissencephaly is observed in three related syndromes characterised by an overmigration of neurons and glial cells into the arachnoid space: Walker–Warburg, Fukuyama and muscle–eye–brain (MEB) syndromes, caused by mutations in genes involved inO‐glycosylation ofα‐dystroglycan.Key ConceptsLissencephaly is defined by a ‘smooth brain’ with absent (agyria) or abnormal wide gyri (pachygyria).Lissencephaly is caused by abnormal neuronal migration during corticogenesis.Neuropathological analysis distinguishes several types of lissencephalies: classical lissencephalies and cobblestone lissencephalies.Classical lissencephalies are caused by mutations inLIS1,DCX,ARXandTubulingenes.Cobblestone lissencephalies are caused by defects inO‐glycosylation ofα‐dystroglycan.Microlissencephalies are caused by dysfunctions of centrosomal‐dependent neuronal progenitor proliferation and of neuronal migration.
Synthetic Biology: Molecular Tools for Engineering Organisms
Authors: Ducat Daniel C 
Published: February 2018

Abstract

Synthetic biology is a biological engineering discipline based on abstracting living systems through the lens of physical engineering concepts. In particular, synthetic biology places an emphasis on the characterisation of simple parts that can be modularly assembled into configurations that give rise to complex, higher‐order behaviours. Within the past two decades, this approach has enabled the development number of new molecular biology tools for modifying living systems in order to investigate fundamental processes or imbuing functions into cells that do not exist in nature. While specific synthetic biology applications span a huge range of seemingly unrelated disciplines (from biofuel producing microbes, to malaria‐resistant mosquitoes, to living medical therapies), these distinct examples derive from reuse and rearrangement of relatively limited set of cell engineering technologies. The continuing development of these core molecular biology tools for controlling gene expression, protein activity and signalling networks can promote evermore ambitious biological engineering projects.

Key Concepts

Synthetic biology is a discipline for biological engineering using principles of physical engineering.

Complex biological systems can be abstracted as a set of core ‘parts’ with separable functions.

A biological part is modular when it confers a discrete function, which can be repurposed and rearranged in many different contexts while maintaining fidelity.

Biological systems naturally display many modular features that are evident at many different scales.

Synthetic biology attempts to identify, characterise and repurpose biological modules to build devices with novel functions.

The field has created several new molecular biology tools for controlling living systems through exploiting the recombination of modular parts.

The tools of synthetic biology are frequently used to imbue organisms with technologically useful traits.

As synthetic biology expands beyond model microbes, its potential to contribute to our fundamental understanding of biology continues to increase.
Stomata
Authors: He Jingjing , Liang Yun‐Kuan 
Published: February 2018

Abstract

As adjustable pores, each delimited by a pair of guard cells, stomata are central determinants of plant photosynthesis, transpirational cooling and ecological adaptability, which have huge impact on global water and carbon cycles, plant competitiveness and nutrients in foods. The specialised guard cell anatomy and membrane ion transport enable plants to adapt stomatal aperture rapidly to hormone and environment changes. In contrast to the highly conserved simple structure across land plants, the stomatal size, density and distribution patterns vary substantially among species or genotypes within a species providing ample genetic resources on which selection can operate. Study of the development and function of stomata is crucial to understand cell fate specification, signal transduction and plant–environment interactions and inform approaches to breed ‘climate change ready’ crop varieties with improved agricultural capacity and food nutrients.

Key Concepts

Stomata and active stomata control are a key evolutionary innovation vital for plants to survive and thrive on land.

Plants use stomata for gas exchange, water regulation, mineral transport, spore dispersal and pathogen defence.

Plants produce stomata in organised patterns and in environmentally optimised numbers.

Stomata vary widely in size and responsiveness among species or genotypes within a species.

The specialised guard cell morphology, anatomy and membrane ion transport enable plants to adapt stomatal aperture rapidly to hormone and environment changes.

Stomata have major influence on the growth and fitness of land plants and global environment as well as food security.

Revealing the molecular nature of stomatal regulators will inform us the approaches to breed climate resilient crops.
Genome‐Wide Approaches to Identify the Interplay of Transcription Factors, Regulatory Elements and Target Genes
Authors: Qu Jieqiong , Zhou Huiqing 
Published: February 2018

Abstract

Tightly controlled gene regulation is essential for embryogenic development and homeostasis. One of the key questions in gene regulation is the interplay between transcription factors, regulatory elements and target genes. Recent development of high‐throughput technologies has made analyses of the complex interplay possible at the genome‐wide scale, and provides insights into the molecular mechanism of gene regulation. These state‐of‐the‐art genome‐wide approaches include RNA (ribonucleic acid)‐seq for gene expression, ChIP‐seq (chromatin immunoprecipitation followed by sequencing) for transcription factor binding and histone modifications, and methods for analysing chromatin accessibility and three‐dimensional chromatin conformation. For each of these approaches, we discuss the background, the current working pipeline and ongoing development. As computational analysis packages and methods are essential for interpreting genome‐wide large data sets, the commonly used ones are summarised with the corresponding technologies.

Key Concepts

The complex interplay of transcription factors,
cis
‐regulatory elements and target genes is essential for proper gene regulation.

RNA‐seq analyses have revolutionised gene expression analyses.

ChIP‐seq analyses assess the binding of transcription factor and the occupancy of histone modifications and provide potential
cis
‐regulatory elements and gene regulation in the genome.

Analyses of chromatin accessibility reveal
cis
‐regulatory elements and complement ChIP‐seq analyses.

Analyses of three‐dimensional chromatin conformation provide information on the chromatin domains that facilitate or restrict gene regulation.
Ancient Population Genomics
Authors: Subramanian Sankar 
Published: February 2018

AbstractRecent advances in genome sequencing technologies and the rapid decline in the cost of sequencing have enabled researchers to study the genomics of ancient populations. In the past decade, ancient population genomic studies led to a number of important discoveries that revealed the (1) relationship between modern and archaic humans such as Neanderthals and Denisovans, (2) contribution of ancient but anatomically modern humans to the ancestry of populations living today, (3) temporal dynamics of ancient population sizes in response to climate change, (4) role of natural selection in shaping the evolution of phenotypes, (5) origins of animal domestication, (6) divergence times between ancient and modern populations and (7) evolution of human pathogens.Key ConceptsAncient population genomics revolutionised our understanding about past evolutionary and demographic events.Rate of evolution could be estimated using time‐stamped ancient samples.Ancient DNA studies revealed the rise and fall of mammalian population sizes in response to climate change.Reconstructing extinct genomes helped to decipher the signatures of genetic admixture between archaic and modern humans.Present‐day Europeans were derived from three ancient human populations.Ancient genomes helped us to understand the role of adaptive evolution in the past.
Wood Decay Fungi
Authors: Kirker Grant T 
Published: February 2018

Abstract

Wood decay fungi are any species of fungi that utilise the structural components of wood as a source of nutrients. They comprise a very diverse group and have a worldwide distribution normally wherever trees are found. Wood decay fungi are vital to ecosystem functioning as they facilitate the decomposition of woody materials into soil. Wood decay fungi are also major contributors to damage to wood in service in both residential and industrial applications, leading to estimated $1B in losses annually. Wood decay fungi have also been exploited for use in industrial processes ranging from product development to waste breakdown. This article focuses on the taxonomic and physiological diversity of wood decay fungi and their importance both on economic and environmental scales.

Key Concepts

Wood decay fungi are a diverse group of microorganisms that are primarily involved in the breakdown of woody biomass.

These fungi are primary drivers of soil formation and nutrient cycling critical to ecosystem function.

Decay fungi also contribute to substantial damage to wood and wood‐based building materials and are a primary consideration in the use of preservative‐treated wood.

Decay of wood by fungi is typically characterised as either white, brown or soft rot with grey rot being a new and emerging distinction among decay fungi.

Collectively, these fungi possess a wide array of physiological mechanisms adapted to break down the structural components of wood.

Both enzymatic and nonenzymatic mechanisms of wood decay have been exploited as industrial processes to break down both man‐made and natural compounds.