bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evolutionary Game Theory
Authors: Broom Mark , Cannings Chris 
Published: November 2010

Abstract

In the natural world, there is a constant struggle between individuals to survive and reproduce; for example, prey compete against their predators and conspecifics compete for resources such as food and territory. The outcomes of these conflicts depend on the strategies adopted by individuals and impact on reproductive success. The theory of evolutionary games, or evolutionary conflicts, addresses the issues of what strategies prevail and coexistence within these competitions under natural selection. The original models were based on competitions between identical conspecifics, although they now cover a huge range of complex behavioural scenarios such as the adoption of elaborate behaviours or costly physical ornaments by male animals seeking mates or the formation of dominance hierarchies among social groups.

Key Concepts:

Strategies are the possible behaviours open to an individual within a game.

Knowing the behaviour of each individual determines the rewards (payoffs) to all individuals in the game.

An evolutionarily stable strategy (ESS) is a strategy that, if played by almost all, resists invasion by any other strategy and so persists through time.

It is possible to have a single ESS, more than one ESS or no ESSs for a given game.

There is the potential for larger payoffs than under an ESS if individuals could co‐operate, but such strategies do not resist invasion and so are unstable.

While there may be more than one ESS, there are important restrictions on which can coexist for simple two‐player conflicts. More complex restrictions apply for multiplayer conflicts, and some of the simpler restrictions of the two‐player conflicts may not apply.

A population composed of individuals playing different strategies is subject to change following evolutionary dynamics, for example, replicator dynamics.

The rest points of evolutionary dynamics are not always the same as the ESSs of a conflict and care must be taken in any specific analysis.

If populations are subject to only small changes in strategy through mutation, change can be modelled by adaptive dynamics.
m
RNA
: Intranuclear Transport
Authors: Politz Joan C Ritland , Pederson Thoru 
Published: November 2010

Abstract

Most genes are transcribed in the nuclear interior and the messenger ribonucleic acid (mRNA) must then move from its transcription site to the nuclear pores to be transported to the cytoplasm for translation. mRNAs interact with multiple proteins both during and after transcription, some of which help to determine their export competency. High‐resolution, live cell tracking studies show that when released from the transcription site, messenger ribonucleoprotein (mRNP) complexes move out into the nucleoplasm in all directions by simple diffusion. The mRNPs sometimes move discontinuously depending on obstacles they encounter and may be corralled in certain regions for a time, but overall, the nascent mRNPs rapidly distribute throughout the entire channel‐like interchromatin space. Export‐competent mRNPs then randomly encounter a nuclear pore and are captured for export to the cytoplasm.

Key Concepts:

mRNPs released from the transcription site move through the nucleoplasm primarily by diffusion.

Diffusing mRNPs can be corralled by encounters with obstacles such as chromatin.

Export‐competent mRNPs randomly encounter nuclear pores and are transported to the cytoplasm.

A minority of mRNAs are transcribed at the nuclear periphery and it is possible that these exit the nucleus through the nearest nuclear pore.
Atherosclerosis: Pathogenesis, Genetics and Experimental Models
Authors: Homeister Jonathon W , Willis Monte S 
Published: November 2010

AbstractAtherosclerosis is a disease of the arteries that results in heart disease and stroke – the most common causes of death in developed countries, and a growing burden in developing countries. Atherosclerosis results from injury to the artery endothelium caused by mechanical and environmental factors, and the resulting inflammatory response in the vessel wall. The location and morphology of the atherosclerotic lesions predict the nature of the resulting vascular disease. Some risk factors for the disease are well known and current therapies are largely directed at modifying them, but the tendency to develop atherosclerosis is determined largely by polygenetic factors that are poorly understood. Recent developments in genetic studies have been applied to atherosclerosis, and are beginning to rapidly reveal the genetic factors that modulate the pathogenesis of this disease.Key Concepts:Atherosclerosis is a common, costly and deadly vascular disease that affects peoples of developed countries, and increasingly burdens developing countries.Atherosclerosis is an inflammatory disease of the arterial vascular wall.The pathogenesis of atherosclerosis is complex, but is generally explained by the ‘response to injury’ hypothesis.Atherosclerotic lesions have varied morphology, and clinical manifestations correlate with lesion type and location.Both environmental and heritable risk factors modulate atherosclerosis development.Candidate gene and linkage analysis studies have failed to identify previously unknown pathways in the pathogenesis of atherosclerosis.Recent publication of the HapMap has made possible genome‐wide association studies aimed at probing the pathogenesis of atherosclerosis.Recent genome‐wide association studies have reproducibly identified several loci involved in the pathogenesis of atherosclerosis, and most of the identified genes are newly implicated in the disease process.APOE‐ or LDLR‐deficient mice are widely used models to study the pathogenesis of atherosclerosis.
Multiple Endocrine Neoplasia Type 2
Authors: Raue Friedhelm , Frank‐Raue Karin 
Published: November 2010

Abstract

Multiple endocrine neoplasia type 2 (MEN 2) is an autosomal dominant hereditary cancer syndrome caused by missense gain‐of‐function mutations of the

RET

proto‐oncogene on chromosome 10. It has a strong penetrance of medullary thyroid carcinoma (MTC) and can be associated with bilateral pheochromocytoma and primary hyperparathyroidism. The specific

RET

mutation may suggest a predilection towards a particular phenotype and clinical course, with strong genotype–phenotype correlations. Recommendations on the timing of prophylactic thyroidectomy and extent of surgery are based on classification of

RET

mutations into risk levels according to genotype–phenotype correlations. By earlier identification of patients with hereditary MTC, the presentation changed from clinical tumours to preclinical disease resulting in a high cure rate of affected patients with much better prognosis.

Key Concepts:

The hereditary cancer syndrome (MEN 2) is caused by germline activating mutations of the
RET
‐proto‐oncogene.

Hereditary medullary thyroid carcinoma (MTC) is the most common manifestation of multiple endocrine neoplasia type 2 (MEN 2) syndrome.

Genetic testing detects nearly 100% of mutation carriers.

Three different clinical variants of MEN 2 are known, MEN 2A, MEN 2B and FMTC.

Each variant of MEN 2 results from different
RET
gene mutations with a good genotype–phenotype correlation.

Recommendation for the timing of prophylactic thyroidectomy and extent of surgery are based on a classification into four risk levels utilising the genotype–phenotype correlation.

If prophylactic thyroidectomy is done at early ages cure rate will be 100% and improves significantly long‐term outcome and prognosis of these patients.

Pheochromocytomas usually present after MTC or concomitantly, rarely it can be the first manifestation of MEN 2A, lifelong annual biochemical screening is necessary in carriers at risk.
DNAHelicase‐deficiency Disorders
Authors: Sidorova Julia M , Monnat Raymond J 
Published: November 2010

AbstractDeoxyribonucleic acid (DNA) helicasesuse energy derived from the hydrolysis of adenosine triphosphate (ATP) to separate the complementary strands of DNA. This article focuses on one family ofDNA helicases, the humanRECQ (recombination) helicasesand the syndromes that arise due to their deficiency. The five humanRECQ helicasesshare a common, conserved helicase domain and all five proteins appear to 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 theRECQ helicase‐deficiency syndromes and the underlying genetics, biochemistry and function of the associated humanRECQ helicasegenes and proteins. We discuss how the loss of RECQ function may promote genetic instability and disease pathogenesis, and howRECQ helicasesmay 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 strands of duplex DNA molecules.RECQ helicases play important roles in many aspects of DNA metabolism including DNA replication and repair, recombination and telomere maintenance.Loss of RECQ helicase function is associated with defects in DNA metabolism, genetic instability, reduced cell proliferation and cellular senescence or apoptosis.Heritable human RECQ helicase deficiencies are rare. Three distinct autosomal recessive RECQ helicase deficiency syndromes have been identified thus far.RECQ helicase‐deficient individuals have an elevated risk of cancer together with additional developmental or acquired findings.Acquired RECQ helicase deficiencies may be common in adult cancer, where loss‐of‐function may modify the response to therapy.
Neural Tube Defects: Genetics
Authors: O'Byrne Michelle R , Au Kit Sing , Northrup Hope 
Published: November 2010

Abstract

Neural tube defects (NTDs) are malformations of the brain and the spinal cord, resulting from lack of closure of the developing neural tube during embryological development. NTDs are complex birth disorders with a worldwide prevalence from 0.5 to 2.0 per 1000 births. The two most common types of NTD are anencephaly and spina bifida, which involve failure of neural tube closure in the cranial and in the back regions respectively. NTDs are hypothesised to be a result of genetic abnormalities and environmental factors; yet, the aetiology remains undetermined. Research studies over the past decade have indicated that maternal folate deficiency is an extremely important risk factor for an NTD birth, with maternal folate supplementation decreasing risk. However, the role that folate plays in NTD risk is not well defined.

Key Concepts:

Neural tube defects (NTDs) are congenital malformations of the brain and spinal cord.

The prevalence rates of NTDs vary worldwide.

NTDs are complex birth defects composed of both genetic and environmental components.

The underlying mechanism remains undetermined.

NTDs are classified by whether they are open or closed and by the location of the lesion.

Folic acid supplementation ameliorates NTD risk.

The majority of NTDs are sporadic and nonsyndromic.

To date, association studies in relatively small patient cohorts have been used in an attempt to find causative genes.

Future additional approaches will include Genome‐Wide Association Study (GWAS) and high‐throughput sequencing.
Genetics of X‐linked Mental Retardation
Authors: Lisik Małgorzata Zofia 
Published: November 2010

Abstract

X‐linked mental retardation (XLMR) refers to a group of inherited disorders characterised by varying degrees of mental retardation, caused by mutations in various genes present on the X‐chromosome. Historically, XLMR is divided into syndromic (MRXS) and nonsyndromic (MRX). At least 209 different XLMR disorders have been described including 143 forms of syndromic mental retardation. Fragile X syndrome is the most frequent syndrome and most studied XLMR syndrome. It is now possible to identify 42% of the genetic defects in XLMR families with obligate female carriers. Most of the mutated genes in XLMR are thought to influence development, cell migration, formation and maintenance of neural networks and cell‐to‐cell communication in brain. Thus the diagnosis of mental retardation in a child has an enormous impact in most affected families. Genetic counselling is strongly recommended to family members.

Key Concepts:

X‐linked mental retardation (XLMR) is a very heterogeneous set of conditions responsible for a large proportion of inherited mental retardation.

XLMR can be divided into syndromic (MRXS) and nonsyndromic (MRX).

Genes involved in XLMR influence development, cell migration, formation and maintenance of neural networks and cell‐to‐cell communication in brain.

Mental retardation phenotype can emerge as the final common pathway of many different types of abnormal cellular processing.

Genetic counselling is an important part in general management in the case of mental retardation.
Sexual Selection: Its Possible Contribution to Recent Human Evolution
Authors: Richards Richard A 
Published: November 2010

AbstractDarwin's appeal to sexual selection in hisDescent of Manwas motivated by the need to explain traits not obviously of survival value – sexually dimorphic and ornamental traits. After Darwin, there was little interest in sexual selection until the 1970s. Since then there has been much progress due to first, what we now know about sexual reproduction and human evolution in general; second, theoretical developments related to runaway processes, parental investment, mating systems and sexual conflicts and cooperation; third, new empirical data about actual mating preferences in humans and closely related species. Three issues have motivated the debates about sexual selection: the explanatory scope of sexual selection; the nature and existence of sexual selection; the relation between naturalsurvivalselection and sexual selection. One recent approach combines survival and sexual selection in the idea that many distinctively human capacities and behaviour are the products of sexual selection on fitness indicators.Key Concepts:The explanatory scopeof a theory or hypothesis is the range of phenomena it can potentially explain.Human fitness indicatorsare those traits that are possible only in highly fit individuals, and are therefore indicative of high fitness.Parental investmentis the amount of resources a parent devotes to the production and care of offspring, in development from the generation of gametes to birth, and to the feeding, education and support of offspring.Sexual selectionis a result of the struggle to reproduce, and is to be distinguished from natural selection and the struggle to survive.Surplus abilitiesin humans are those abilities not obviously explainable in terms of naturalsurvivalselection and advantages for survival, such as we see in advanced mathematics, poetry, dancing, music and more.
Rho
GTPase
Function in Cell Morphogenesis
Authors: Pedersen Esben , Brakebusch Cord 
Published: November 2010

Abstract

Cell morphogenesis is the development of a specific cell morphology, which includes the acquisition of cell shape, cell polarity, cell–cell and cell–ECM (extracellular matrix) contacts. Cell morphogenesis is dependent on the interaction of the cell with its environment and therefore not a cell autonomous process. Crucial for cell morphogenesis is the regulation of the
actin
cytoskeleton. Furthermore, regulation of gene expression and activation of different intracellular signalling pathways contribute to cell morphogenesis. Rho
guanosine triphosphatases
(GTPases) are master regulators of the
actin
cytoskeleton, which affects cell shape and the position of integrins and cadherins,
actin
cytoskeleton attached cell surface receptors. In addition, Rho GTPases regulate endocytosis, vesicle transport, secretion and gene expression. Not surprisingly, therefore, this family of molecules was found to be particularly important for cell morphogenesis.

Key Concepts:

Rho GTPases are signal integrators.

Rho GTPases have overlapping functions.

Rho GTPases regulate cell shape by controlling remodelling of the actin cytoskeleton.

Cdc42 regulates different aspects of cell polarity in a cell type‐specific manner.

Rho GTPases regulate cell adhesion to the extracellular matrix and to other cells.
Climate Change Impacts: Insects
Authors: Stange Erik E , Ayres Matthew P 
Published: November 2010

Abstract

Climate exerts powerful effects on the distribution and abundance of the earth's insect species, and we should expect climate warming to generate changes for many insect populations and the ecosystems they inhabit. A substantial scientific literature provides a foundation for describing how insect species are responding to recent climatic trends on the basis of insect physiology, and predicting generalised species distributions and population dynamics for the future. Warmer temperatures generally lead to more rapid development and survival in insects in mid‐ to high latitudes, which can account for detectable and unambiguous shifts in a range of insect species over the past half century. Increased warmth also advances the onset of insect life cycles for the many species that use thermal cues to match the timing of life history events with the changing seasons. Owing to their relatively short life cycles, high reproductive capacity and high degree of mobility, insects’ physiological responses to warming temperatures can also generate particularly large and rapid effects on species population dynamics.

Key Concepts:

Warmer temperatures associated with climate changes will tend to influence (and frequently amplify) insect species’ population dynamics directly through effects on survival, generation time, fecundity and dispersal.

Individual insect species’ responses to climate change, however, will depend on their geographic range, trophic level and natural history.

Insect populations in mid‐ to high latitudes are expected to benefit most from climate change through more rapid development and increased survival. Much less is known about the effects of increased warming on tropical insect species.

Insect species’ mortality may decrease with warmer winter temperatures, thereby leading to poleward range expansions.

The physiological effects of climatic warming on insects species can also act indirectly through trophic interactions (i.e. host plants and natural enemies).

Insects feature prominently among the documented range expansions that illustrate biological responses to recent climate change.

Because insect species in general have relatively short life cycles, high reproductive capacity and high degree of mobility, the physiological responses to warming temperatures can produce large and rapid effects on species population dynamics.
Barcoding South American Birds
Authors: Lijtmaer Darío A , Tubaro Pablo L 
Published: November 2010

AbstractDNA barcoding, a genetic‐based species identification system, has proven to be highly effective. The project to barcode all the birds of the world was one of the first campaigns to be launched and over 30% of the species have been already barcoded. The Neotropics are the most biodiverse region of the planet, including almost 4000 species of birds, and barcoding its avifauna is therefore vital for the project. Most of the progress within this region has been made in South America, including the first large‐scale barcode study of Neotropical vertebrates, which is being carried out in Argentina. This study has shown that barcoding is highly efficient in the southern Neotropics, allowing the recognition of more than 98% of bird species. Large‐scale barcoding surveys also allow flagging interesting species or groups of species worthy of deeper analysis, studying avian diversification and analysing continental patterns of evolution, biogeography and speciation.Key Concepts:DNA barcoding is a system for species identification that is based on the use of a short, standardised DNA fragment (COI in the case of animals).The All Birds Barcoding Inititative (ABBI) is the campaign that aims to barcode all the birds of the world, and approximately 30% of the species have been already barcoded.The Neotropical region is the most biodiverse of the Planet, including almost 4000 bird species, and barcoding its avifauna is therefore vital for the advancement of the ABBI.Most of the progress in the Neotropics has been made in South America, where a large‐scale project to barcode the Birds of Argentina is being performed.Barcoding has proven to be highly efficient for species recognition in the southern Neotropics, where more than 98% of bird species can be identified using COI.Barcoding the Argentine avifauna also flagged many interesting species or groups of species worthy of further analysis, including approximately 5% of species in which at least two deeply diverging lineages were found.The study of avian diversification patterns in the region using COI showed cases of allopatric, paraptric and sympatric divergences.The comparison of the COI datasets between the southern Neotropics and the Nearctic suggests that species are slightly older in the former and supports the notion that phylogenetic structuring is more complex in the Neotropics.
Evolution of Immune Proteins in Insects
Authors: Bulmer Mark S 
Published: November 2010

AbstractInsect immune proteins evolve more rapidly than nonimmune proteins. Based largely on genetic studies inDrosophilaspecies, this elevated rate appears to be due to adaptive evolution in only a small subset of immune proteins. The genetic signature of adaptive evolution is apparently a response by the host to interference or evasion of the immune system by pathogens, which are usually unknown. In contrast, many insect immune proteins appear to be constrained not to change because they interact with conserved molecular targets in a pathogen's cell wall or plasma membrane. Adaptive immune protein evolution may be attributable to a sustained arms race between host and pathogen or to rapid environmental change that exposes insects to new pathogen suites. Evidence of a correlation between the strength of selection and functional divergence in antimicrobial peptides provides confirmation that the inferred genetic signatures of adaptive evolution reflect a response to pathogen selective pressure.Key Concepts:A small set of immune proteins inDrosophilaevolve much more rapidly than other proteins.Insect antiviral proteins of the RNA interference system are among the top 3% of rapidly evolving proteins inDrosophila.There is surprisingly little evidence of adaptive evolution inDrosophilaantimicrobial peptides.Many receptors and effectors of the insect immune system appear to be evolutionary constrained due to their interaction with conserved target molecules.Pathogens target certain vulnerable immune proteins for suppression and positive selection in these proteins appears to reflect a counter response to this suppression.The selective pressure imposed by pathogens appears to be greater for social than nonsocial insects.Rapid changes in the types of pathogen that hosts encounter as well as long‐term co‐evolutionary arms races may drive adaptive immune protein evolution.Positive selection appears to drive the functional divergence of antimicrobial peptides in termites and other animals.