bluuebunny/crossref_metadata_2025_split huggingface dataset:
Somitogenesis in Vertebrate Development
Authors: Bailey Charlotte , Dale Kim 
Published: June 2015

Abstract

A segmented body plan is a conserved feature of all vertebrate species and is established early in embryonic development by the formation of somites, the precursors to the skeleton, musculature and dermis. These epithelialised structures are formed with a species‐specific periodicity during the process of somitogenesis. Gathering evidence suggests that somitogenesis is regulated by a molecular oscillator mechanism that, together with a morphogenic gradient, stipulates when and where somites form. Mutations in key molecular players in this mechanism have been closely linked to developmental disorders and segmental malformations. It is therefore of great medical interest to elucidate the regulatory mechanisms which govern this key developmental process, much of which is still not yet fully understood.

Key Concepts

A segmented body plan is a conserved feature of all vertebrate species.

Somitogenesis describes the periodic formation of somites, which is the first overt sign of segmentation to appear in the embryonic vertebrate body plan.

The temporal periodicity of somitogenesis is thought to be regulated by a molecular oscillator mechanism termed the segmentation clock.

There is emerging evidence to suggest a significant degree of conservation of the regulatory mechanisms governing somitogenesis in different vertebrate species.

Some particular disease states characterised by segmentation defects have been shown to result from mutation in key Notch‐regulated components of somitogenesis.

Many of the mechanisms thought to regulate somitogenesis and somite boundary formation appear to be highly reliant on the Notch signalling pathway.

There is a large degree of crosstalk between the Notch, Wnt and FGF signalling pathways that orchestrate somitogenesis.

Future advances in our understanding of the regulatory mechanisms governing somitogenesis rely on developing mathematical models and interdisciplinary approaches to direct and cooperate with biological investigation.
HoxGenes: Embryonic Development
Authors: Montavon Thomas 
Published: June 2015

AbstractHoxgenes encode a family of transcription factors responsible for the establishment of the animal body plan. Their organisation in genomic clusters is conserved during evolution and is instrumental in defining the domain of activity of each gene in the embryo: the place and time ofHoxgene expression is dictated by the position of each gene within the cluster. A unique set ofHoxgenes is active at each axial level along the embryonic anterior to posterior axis. These diverse complements of Hox proteins determine morphological identities by controlling the transcription of specific target genes. Changes inHoxgenes number, expression and function likely participated in morphological diversification during animal evolution.Key ConceptsHoxgenes determine the identity of structures along the anterior–posterior embryonic axis.Hoxgenes are widely conserved among animal species and are organised in genomic clusters.Colinearity is the correspondence between the order ofHoxgenes within the cluster and their time and place of expression along the embryonic axis.Loss or gain of function ofHoxgenes lead to homeosis, the morphological transformation of a body structure into another one.Hox proteins regulate specific sets of target genes by interacting with dedicated cofactors.Hoxgene regulation integrates multiple inputs via complex sets of local and long‐range cis‐acting regulatory elements.Chromatin modifiers of the Polycomb and Trithorax families are critical in controlling the onset and maintenance ofHoxgene transcription.Changes inHoxgene expression and function accompanied major morphological transitions during animal evolution.
Pathogen Resistance Signalling in Plants
Authors: Corrion Alex , Day Brad 
Published: June 2015

Abstract

Within natural ecosystems, most plants are resistant to most pathogens. At a fundamental level, this seemingly simply truth may hold the key to our understanding of how plants have evolved to survive under a myriad of environmental conditions and their associated stresses. Indeed, in defining how plants evolve, adapt and maintain broad spectrum resistance to most pathogens – typically referred to as non‐host resistance – we may not only reveal the mechanisms that underpin plant resistance signalling but also the precise manner in which plants regulate these processes under various environmental conditions. Herein lies the greatest challenge and unanswered question in the field of agriculture today:
How do we feed 9 billion people by the year 2050?
To address this, one of the first hurdles that must be overcome is a full understanding of the processes that regulate stress (i.e. abiotic and biotic) signalling in plants, as well as the processes that define pathogen and host specificity, including the performance of these processes under rapidly changing environmental conditions. In the case of pathogen infection, plants utilise a broad suite of innate and inducible mechanisms to resist invasion. In large part, these processes are governed by the activity of resistance (R) proteins, which are evolutionarily conserved and highly evolved proteins that function not only in pathogen recognition but also in the activation of the cellular processes necessary to defend against proliferation and the elicitation of disease. Furthermore, recent data supports the hypothesis that numerous processes, such as the balance between growth and defence, also contribute to the host resistance and pathogen virulence.

Key Concepts

Most plants are resistant to most pathogens.

Modern agriculture practices positively impact crop yield and durability. These practices can also have a negative impact on the unintended selection and enrichment of virulent pathogens.

Plants defend against pathogen invasion using a suite of highly conserved resistance (
R
) genes.

Pathogens have evolved to recognise and respond to the activity of plant R proteins through the deployment of secreted virulence factors.

Immune signalling in plants utilises various pre‐formed and inducible processes to defend against pathogen infection.

Many basic physiological processes, including response to light, temperature and water availability, are associated with, and required for, immune signalling.

The development of advanced genome sequencing technologies has increased the speed at which the development and selection of elite breeding lines are deployed into cropping systems.

Current plant breeding approaches utilise a hybrid of molecular genomics and classical breeding techniques to identify and introduce desirable traits into crops to enhance plant performance (e.g. resistance) and yield.
Retroviral Pseudotypes – From Scientific Tools to Clinical Utility
Authors: Temperton Nigel J , Wright Edward , Scott Simon D 
Published: June 2015

Abstract

Retroviral pseudotypes are important research and diagnostic tools for basic and clinical virology studies, facilitating the detailed investigation of individual genes, cellular receptors, antibody responses, serosurveillance and antiviral therapies. Importantly, pseudotypes enable the study of highly pathogenic viruses, without the need for high containment. Their use as gene therapy vectors is widely documented, but other uses, once less well known, are becoming more prominent. The substitution of envelope proteins expressed on the virion surface enables pseudotypes to be employed as surrogates for wildtype viruses in antibody neutralisation or antiviral screening assays and for the study of cell–virus receptor interactions. In addition, they are increasingly being utilised as vaccine immunogens, expressing the antigen either on the particle surface or as a transfer gene for cellular expression. These studies demonstrate the potential for using pseudotypes for both scientific and clinical applications.

Key Concepts

Students will learn:

What are retroviral pseudotypes.

How they are constructed and titrated.

The common elements that comprise a retroviral pseudotype.

How retroviral pseudotypes can be used to deliver genes.

How they can be used as tools for the study of viral attachment, entry and receptor identification.

About using pseudotypes as surrogate viruses in antibody neutralisation assays.

The use of pseudotypes to measure vaccine immunogenicity and screen for antiviral activity and resistance.

How pseudotypes can be used as experimental vaccines.
Coltiviruses and Seadornaviruses
Authors: Mohd Jaafar Fauziah , Attoui Houssam 
Published: June 2015

Abstract

Coltiviruses and seadornaviruses are members of the family
Reoviridae
, which encompasses alongside the genera
Coltivirus
and
Seadornavirus
, 13 other genera of viruses that can infect mammals, birds, aquatic animals, reptiles, insects, plants, fungi and protists. Coltiviruses are transmitted by hard ticks of the family
Ixodidae
, whereas seadornaviruses are mosquito‐borne. These viruses can infect humans, following the bite of adult infected female ticks or mosquitoes, causing febrile illnesses and are occasionally responsible for encephalitis. Coltiviruses are principally endemic in the north‐western parts of the United States and Canada and were also reported in European countries, including France and Germany. Antibodies to coltiviruses have also been identified from patients in the former Czechoslovakia and South Korea. Seadornaviruses are principally endemic in the south‐east Asia, although recent data showed that there has been an expansion of their distribution northwards, reaching the north‐western Chinese borders. Banna virus (
Seadornavirus
) has been isolated from human encephalitis cases.

Key Concepts

Coltiviruses are transmitted by adult female tick (family
Ixodidae
) bite and have animal reservoirs.

Coltiviruses can infect humans causing febrile illnesses and can cause encephalitis in rare cases.

Seadornaviruses are transmitted by mosquitoes and no animal reservoir is known to date.

Seadornaviruses can infect animals and humans causing febrile illnesses and were reported to be responsible for cases of encephalitis.

Coltiviruses show an evolutionary relationship to the turreted mycoreoviruses, aquareoviruses and orthoreoviruses.

Seadornaviruses show an evolutionary relationship to the nonturreted rotaviruses.

Coltiviruses seem to represent a missing link between turreted and nonturreted members of the family
Reoviridae
.

Differential diagnostic serological and molecular assays for coltiviruses and seadornaviruses are available.

Structure of the viral particles of Banna virus shows striking similarities to that of the rotaviruses.
Virus‐Induced Human Oncogenesis
Authors: Bedi Manmeet S , Ploubidou Aspasia 
Published: June 2015

Abstract

Infectious agents are estimated to contribute to oncogenesis in
c
. 25% of human cancers worldwide. Approximately half of them are attributed to infection by oncogenic viruses. Viruses are obligatory intracellular pathogens, which disrupt host cell homeostasis during their life cycle. The induction of malignancy is not part of their life cycle, but rather a multistep outcome, that may occur several years after the infection. Oncogenesis is initiated by the disruption of cellular mechanisms (detecting and repairing DNA damage, activating checkpoints and inducing apoptosis or survival) through the activity of viral proteins. Host and environmental factors further contribute to the multistep aetiology of cancer development and progression. This article describes the common molecular mechanisms by which human oncogenic viruses disrupt cell homeostasis and the prophylactic and therapeutic treatment options for virus‐induced malignancies and discusses the identification of emerging oncogenic infectious agents.

Key Concepts

Oncogenic viruses are estimated to contribute to approximately 15% of all human malignancies.

Human oncogenic viruses include both DNA viruses (EBV, HPV, MCV, HBV and KSHV) and RNA viruses (HCV and HTLV‐1).

Induction of malignancy is not part of the viral life cycle and confers no benefit to the virus per se.

Oncogenic viruses disrupt host cellular pathways (DNA repair mechanisms, cellular checkpoints and apoptosis) for efficient viral replication, consequently initiating cancer development.

Viral oncogenesis is a multi‐step process, initiated by the action of viral proteins but requiring additional factors for disease development and progression.

Transmission of oncogenic viruses takes place mainly via human contact including, but not limited to, sexual transmission.

Prophylactic (vaccine) treatment options are limited. Therapeutic treatments include anti‐virals in combination with chemotherapy and surgical removal of the tumours.

Emerging oncogenic viruses comprise a growing group of newly identified viruses with putative oncogenic potential, which have been detected in association with human cancers.
Togaviruses
Authors: Powers Ann M 
Published: June 2015

AbstractThe viruses of the familyTogaviridaeare an extremely diverse group. There are two genera in the family:AlphavirusandRubivirus.Rubiviruscontains a single member (rubella virus) while there are 31 distinct members in the genusAlphavirus. The alphaviruses are typically transmitted by arthropods, primarily mosquitoes, whereas rubella virus is transmitted via respiratory secretions. The togaviruses have a nearly global distribution, cause a wide range of illness in humans and other animals, and have multiple mechanisms of pathogenesis. Interestingly, while the viruses are genetically extremely simple, the disease they cause ranges from mild or asymptomatic illness to severe polyarthralgia to encephalitis. This work summarises the current understanding of togavirus epidemiology, transmission and pathogenesis and describes current and future options for control of these pathogens.Key ConceptsTogaviruses are an exceptionally diverse group of viruses with global distribution, a wide array of clinical disease, and distinct modes of transmission.While sharing genome functional elements and general virion structure, viruses of the generaRubivirusandAlphavirushave few other common features.Alphaviruses are continuing to emerge in new ecological and epidemiological patterns.Despite a widely available and efficacious vaccine, rubella virus persists as a global health concern.More investigations are required to understand the pathogenesis of the vast range of alphaviruses.
Bayh‐Dole
Authors: Winickoff David E , Valdivia Walter D 
Published: June 2015

Abstract

Bayh‐Dole is shorthand for the public policy in the United States that allows universities to take title to patents on discoveries made from state‐funded research. The Bayh‐Dole Act, enacted by the US Congress in 1980, has been emulated in many countries around the world for its putative benefits on national rates of innovation and has exerted a profound influence on university patenting practices in the United States and abroad. Bayh‐Dole has contributed to the sharp increase in university patenting activity. Its impact on the innovation system as a whole is harder to measure and has been the subject of scholarly and political controversy. While proponents of this policy argue that it has injected American innovation with new dynamism, other analysts have cast doubt on the economic benefits of Bayh‐Dole. Furthermore, there are concerns that the Act negatively effects academic cooperation and runs against the public mission of universities.

Key Concepts

Technology transfer is the dynamic exchange of knowledge among universities, industry and governmental agencies.

Bayh‐Dole regulates intellectual property aspects of university technology transfer.

The Bayh‐Dole policy of facilitating university ownership of state‐funded discoveries has been emulated in many countries, which has helped increase the rates of university patenting in the United States and abroad.

Increased rates of patenting per se are not indicators of increased rates of new product development and new economic activity.

The actual effects of Bayh‐Dole on the innovation system are hard to measure and the subject of scholarly and political controversy within the United States and elsewhere.

Patenting and licensing constitute just one of many modes of university technology transfer, which also occurs
inter alia
through student training, collaborative research agreements, dissemination of new knowledge through publication and public talks.

Bayh‐Dole has become a lightning rod for debates about the commercialisation of research and higher education reform.
Genetics of Non‐alcoholic Fatty Liver Disease
Authors: Kovac Ursa , Rozman Damjana 
Published: June 2015

Abstract

Non‐alcoholic fatty liver disease (NAFLD) is a complex and widely prevalent liver disorder, traditionally characterised by pathological changes ranging from simple steatosis to non‐alcoholic steatohepatitis (NASH) that can further progress to cirrhosis and hepatocellular carcinoma. Owing to the epidemics of obesity and metabolic syndrome, NAFLD is the most frequent liver disorder in the Western world. It is considered to be a multifactorial state, leading not only to liver related mortality but also to increased cardiovascular, type 2 diabetes mellitus and the overall mortality. The natural course of NAFLD is highly variable and is influenced by both environmental and genetic factors. Candidate gene and genome wide association studies together with other clinical data reveal the importance of genetic factors in susceptibility to NAFLD where polymorphisms in genes involved in the control of insulin resistance, lipid metabolism, inflammation and oxidative stress are linked to the progression of liver damage. To date, polymorphisms in
PNPLPA3
, the patatin‐like phospholipase domain containing 3 gene, remain the most consistent genetic association with NAFLD while a number of other genetic polymorphisms have been associated with the disease in case–control studies. It is now necessary to explore the molecular mechanism underlying associations between gene variants and pathogenesis of various stages of NAFLD.

Key Concepts

NAFLD is a complex disease influenced by both genetic and environmental factors which interact to determine the disease phenotype and its progression.

The pathogenesis of NAFLD remains poorly understood. It is under debate if the development of simple steatosis and NASH is the result of two or multiple hits, or whether it is a more complex network phenomenon.

Susceptibility to and progression of NAFLD differ according to race, ethnicity, gender and lifestyle.

Several SNPs in the human genome associate with susceptibility to and progression of NAFLD.

The most consistently replicated genetic risk factor for NAFLD disease is the rs738409 polymorphism in the human
PNPLA3
, the patatin‐like phospholipase domain containing gene 3, also called adiponutrin.

Other SNPs in genes influencing lipid metabolism, insulin resistance, inflammation, oxidative stress, extracellular matrix synthesis, degradation, apoptosis, and so on associate with NAFLD; however, they require conformation before being formally associated with NAFLD stages.
Collective Cell Migration in Neural Crest Development
Authors: Theveneau Eric , Andrieu Cyril 
Published: June 2015

Abstract

The migration of multiple cells as a cooperative unit known as collective cell migration is a common phenomenon in development, cancer and healing. Cooperation can be implemented by physical and/or chemical means and thus happens in epithelial as well as mesenchymal cell populations. Neural crest cells, a highly motile embryonic population, are a well‐known model for epithelial–mesenchymal transition and cell migration. Neural crest cells use various strategies to cooperate and migrate collectively which make them a good model for the study of collectiveness. Further, neural crest cells' interaction with other embryonic populations also relies on cell cooperation, thus providing a model for the study of cell cooperation during organogenesis.

Key Concepts

Neural crest cells are migratory multipotent stem cells.

Neural crest cells distribute according to cell–cell and cell–environment interactions.

Some neural crest cell populations migrate collectively.

Collectiveness is based on cell–cell cooperation via paracrine chemotaxis and cell–cell adhesion.

Collectiveness influences cell guidance.

Cooperation takes place at several orders of magnitude: among neural crest cells and between neural crest cells and adjacent cell populations.
Joseph Henry Woodger
Authors: Nicholson Daniel J , Gawne Richard 
Published: June 2015

Abstract

Joseph Henry Woodger (1894–1981) was one of the foremost theoretical biologists of the twentieth century. Starting out his career as an experimental embryologist and cytologist, Woodger became increasingly interested in the conceptual foundations of biology. Eventually, he abandoned all empirical research so that he could devote himself fully to studying the structure of biological theories. Perhaps his major accomplishment was the 500‐page treatise
Biological Principles: A Critical Study
(1929), which systematically investigated the epistemological basis of biological knowledge through an analysis of its central concepts. Today, he is mostly remembered for his audacious monograph
The Axiomatic Method in Biology
(1937), which remains the most ambitious attempt to reformulate the propositions of biology (especially genetics, embryology, and taxonomy) using the tools of symbolic logic and pure mathematics. Woodger is also known for establishing the Theoretical Biology Club, and for introducing the ‘Bauplan’ concept into Anglophone biology. The insect
Terpandrus Woodgeri
(Woodger's Gumleaf Katydid) is named in his honour.
Transposons in Eukaryotes (Part
A
): Structures, Mechanisms and Applications
Authors: Wang Zhenxing , Kunze Reinhard 
Published: June 2015

Abstract

Transposable elements (TEs) are DNA (deoxyribonucleic acid) segments which can mobilise from their original location and (re)insert into new positions in the genome. TEs occur in almost all eukaryotic genomes. Half of the human genome consists of TEs and large plant genomes are composed of more than 80% TEs. Prevailing among these are the retrotransposons (class I elements) that propagate through an RNA (ribonucleic acid) intermediate. DNA transposons, or class II elements, move as DNA by a cut‐and‐paste mechanism. The vast majority of transposon insertions into genes result in gene damage. It is therefore of ‘mutual interest’ of host cells and transposons to limit transpositions to very low frequencies. Eukaryotes normally keep transposons under control by epigenetic inactivation via transcriptional and post‐transcriptional gene silencing. However, in rare cases, transposon insertions also lead to altered gene regulation or to the development of novel cellular functions, a process termed ‘domestication’ of transposons. In genetic research, TEs are used as versatile tools for insertion mutagenesis and gene isolation.

Key Concepts

Transposons are evolutionary old components of almost all eukaryotic genomes.

Transposon contents in eukaryotic genomes vary from <1% to >85%.

By default, all transposons in a genome are epigenetically silenced by DNA (deoxyribonucleic acid) and histone modification.

Environmental stress (‘genome shock’) can lead to release of epigenetic silencing and reactivation of transposons.

Transposon insertions into genes are almost always deleterious, but in rare cases can result in novel gene regulation patterns.

Very rarely transposons were ‘domesticated’ to provide novel functions to the host.

Transposons can be applied as genetic tools for mutagenesis and gene isolation.