bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rupture Directivity of the Strongest 2016–2017 Central Italy Earthquakes
Authors: Calderoni Giovanna , Rovelli Antonio , Di Giovambattista Rita 
Published: October 2017

AbstractThe along‐strike rupture directivity of 16 of the strongest earthquakes (4.4 ≤ Mw ≤ 6.5) within the 2016–2017 central Italy seismic sequence is estimated by investigating high‐frequency S wave amplitude variations versus source azimuths with an empirical Green's function deconvolution approach. The results confirm that an along‐strike rupture directivity is a persistent feature of normal‐faulting earthquakes in the Apennines. The preferred rupture directions of the 2016–2017 earthquakes and of similar‐magnitude events from the 1997 Umbria‐Marche and 2009 L'Aquila‐Campotosto seismic sequences show a significant spatial consistency. Different sectors of the Apennines show an alternating trend of preferential along‐strike rupture propagation directions with significant spatial and temporal stabilities independent of the magnitude. These results, if confirmed by further data, could lead to more refined hazard assessments of the investigated region.
Multiscale Characterization of Joint Surface Roughness
Authors: Nigon Benoit , Englert Andreas , Pascal Christophe , Saintot Aline 
Published: October 2017

AbstractRecent studies provided detailed characterizations of fault (i.e., shear fracture) roughness at different length scales. Similar investigation for joints (i.e., tensile fractures) are seldom and not as detailed. The present study aims at characterizing joint plumose patterns. We investigated the scale‐dependent surface roughness properties of S‐type plumoses. Joint surface measurements at relatively large scales were carried out with Light Detection and Ranging (LiDAR) technology. Joint surface measurements at the microscopic scale were carried out based on a noncontact optical method, using a Keyence VHX‐2000D microscope. Three parameters were used to characterize fracture surface elevation, standard deviation, Hurst exponent, and correlation length through 3 scale length orders of magnitude. Our study showed that standard deviation and correlation length decrease with scale, similarly to previous findings on faults. In addition, the range of Hurst exponents as a function of scale for the studied joint surface agrees well with those previously found for faults. However, directional analysis showed that correlation length and Hurst exponent of joint surfaces at scales smaller than 1 dm differ significantly from the ones of fault surfaces. In contrast to fault surface ornaments that are mainly characterized by linear structures, plumose structures show marked variability in orientation and anisotropy as a function of position on the joint surface.
Effective Pressure Law for the Intrinsic Formation Factor in Low Permeability Sandstones
Authors: Chen M. , Li M. , Bernabé Y. , Zhao J. Z. , Zhang L. H. , Zhang Z. Y. , Tang Y. B. , Xiao W. L. 
Published: October 2017

AbstractThe effective pressure law for the intrinsic formation factor of low permeability sandstones from the Ordos Basin (northwest of China) was studied experimentally by measuring the electrical resistivity of brine saturated rock samples while cycling the pore and confining pressures, pp and pc. We used a 100,000 ppm NaCl solution so that the results could be directly interpreted in terms of the intrinsic formation factor F. The Response Surface method was used to construct a quadratic function of pp and pc fitting the experimental data, from which the coefficient α of the effective pressure law, peff = pc – αpp, was determined. We found that the coefficient α generally had low values, mainly from 0.2 to 0.4, thus contradicting the theoretical prediction that α should be equal to 1 for scale‐invariant properties, such as F, in linear elastic materials having a homogeneous solid matrix. Since the two underlying assumptions, linear elasticity and homogeneity of the solid matrix, are likely violated in reservoir rocks, we tried to assess their effects on α using simple analytical models, based on idealized geometries of the pore and solid phases. Analysis of these models suggests that non‐linear elasticity associated with the formation of solid–solid contacts in the compressed rocks (e.g., during closure of rough cracks or crack‐like pores along the grain boundaries), may be more effective in producing the low α values observed than inhomogeneity of the solid matrix.
Alternating Influence of Northern Versus Southern‐Sourced Water Masses on the Equatorial Pacific Subthermocline During the Past 240 ka
Authors: Rippert Nadine , Max Lars , Mackensen Andreas , Cacho Isabel , Povea Patricia , Tiedemann Ralf 
Published: October 2017

AbstractThe eastern equatorial Pacific (EEP) is a key area to understand past oceanic processes that control atmospheric CO2 concentrations. Many studies argue for higher nutrient concentrations by enhanced nutrient transfer via Southern Ocean Intermediate Water (SOIW) to the low‐latitude Pacific during glacials. Recent studies, however, argue against SOIW as the primary nutrient source, at least during early Marine Isotope Stage 2 (MIS 2), as proxy data indicate that nutrients are better utilized in the Southern Ocean under glacial conditions. New results from the subarctic Pacific suggest that enhanced convection of nutrient‐rich Glacial North Pacific Intermediate Water (GNPIW) contributes to changes in nutrient concentrations in equatorial subthermocline water masses during MIS 2. However, the interplay between SOIW versus GNPIW and its influence on the nutrient distribution in the EEP spanning more than one glacial cycle are still not understood. We present a carbon isotope (δ13C) record of subthermocline waters derived from deep‐dwelling planktonic foraminifera Globorotaloides hexagonus in the EEP, which is compared with published δ13C records around the Pacific. Results indicate enhanced influence of GNPIW during MIS 6 and MIS 2 compared to today with largest contributions of northern‐sourced intermediate waters during glacial maxima. These observations suggest a mechanistic link between relative contributions of northern and southern intermediate waters and past EEP nutrient concentrations. A switch from increased GNPIW (decreased SOIW) to diminished GNPIW (enhanced SOIW) influence on equatorial subthermocline waters is recognized during glacial terminations and marks changes to modern‐like conditions in nutrient concentrations and biological productivity in the EEP.
Characterization and Mitigation of Radio Frequency Interference in PolSAR Data
Authors: Tao Mingliang , Zhou Feng , Zhang Zijing 
Published: October 2017

AbstractPolarimetric synthetic aperture radar (PolSAR) is a very important instrument for active remote sensing. However, it is common to find that PolSAR echoes are often contaminated by incoherent electromagnetic interference, which is referred to as radio frequency interference (RFI). The analysis of RFI signatures and its influence on PolSAR data seems to be lacking in existing literatures, especially for PolSAR post products, such as the polarimetric decomposition parameters and clustering result. The goal of this paper is to reveal the link between RFI and polarization, as well as to analyze the impact of interference on PolSAR image and its post products. Qualitative and quantitative analyses of the adverse impact of RFI on the real measured NASA/Jet Propulsion Laboratory (JPL) Uninhabited Aerial Vehicle Synthetic Aperture Radar data set are illustrated from two perspectives, that is, evaluation of imaging quality and interpretation of scattering mechanisms. The point target response and effective number of looks are evaluated for assessing the distortion to focusing quality. Further, we discussed the characteristics of ultra wideband RFI and proposed a mitigation method using nonnegative matrix factorization along azimuth direction. The experimental results indicate the effectiveness of the proposed method.
Plant Virus Diseases: Epidemiology
Authors: Navas‐Castillo Jesús , Fiallo‐Olivé Elvira 
Published: October 2017

Abstract

The epidemiology of plant virus diseases concerns the cyclical development of virus diseases within plant populations in time and space. It also deals with how and why a virus is spread by vectors in an ecosystem. The main factors that influence the epidemiology of plant virus diseases involve the viruses, the plant hosts and the vectors. The interactions between these factors are complex and depend on the species, strain and isolate of the virus, its host range and the ability of the vector to disseminate the virus. All components of the epidemiological process of a plant virus are influenced by the environmental conditions, both biotic and abiotic, which can determine the successful development of an epidemic. Knowledge of these factors is fundamental to the choice and improvement of control methods to prevent or eliminate plant virus diseases.

Key Concepts

Plant viruses are a concern for agriculture as virus diseases can cause qualitative and/or quantitative losses of yield.

Modern agriculture has caused the dissemination of exotic plant species, viruses and vectors into foreign environments.

The emergence of novel virus species and strains has been increasing worldwide in the past two decades.

Most plant viruses are transmitted by vectors, mainly insects.

A noticeable number of plant viruses have been found to pass from one generation to the next through seed.

Weeds and other wild plants play a key role as alternative virus reservoirs and as a source of novel viruses which can potentially infect crops.

Environmental factors, both physical and biotic, may affect the infection cycle at different grades.

Understanding of epidemiological processes is fundamental to the choice and improvement of control methods to eliminate the diseases that viruses cause.

Control strategies basically focus on the elimination of virus sources and the avoidance of spatio–temporal coincidences between viruses, vectors and crops.
Genetic Epidemiology of Complex Traits
Authors: Rana Brinda K , De Vivo Imaculata , Schork Nicholas J 
Published: October 2017

Abstract

Genetic epidemiology is a research discipline that combines genetics, molecular biology, epidemiology, statistics and bioinformatics to investigate the role of genes, the environment and their interaction in the expression of quantitative and qualitative traits and diseases in the population at large. Genetic epidemiologists often leverage population‐based family, case–control, and cohort research designs, including many with a longitudinal data collection scheme. However, characterising the influence of genes and the environment traits and diseases is complicated because most traits and diseases are influenced by a number of genetic and nongenetic factors. In addition to the problems associated with the characterisation of the genetic and environmental factors influencing traits and diseases due to the complex, multifactorial and context‐dependent pathophysiological basis of most traits and diseases, a number of issues associated with the genetic structure of human populations also complicate relevant analyses. Genetic epidemiologists attempt to deal with these issues in many ways. As the current biomedical research area era involving high‐throughput and data‐intensive assays evolves, new fields (e.g. metabolomics, epigenomics and megagenomics), technologies (e.g. high‐throughput sequencing, microarrays and mass spectrometry) and statistical approaches will be brought into genetic epidemiology, enabling more comprehensive ‘system‐level’ approaches to characterising the roles of the environment and inherited factors in disease risk, incidence, prevalence and response to therapy.

Key Concepts

Genetic epidemiologists investigate the role of genes, the environment and their interaction between the aetiology and population‐level incidence and prevalence of health‐related traits and diseases within families and in the population at large.

Factors at both the population and the individual or pathophysiological level contribute to the complexity of complex diseases, making it difficult to identify and characterise their determinants.

The main approaches taken by genetic epidemiologists for discovering genes influencing diseases and traits are family‐based linkage and population‐based association studies.

Once a variant gene has been identified, genetic epidemiologists characterise the effect of that gene on the disease burden or trait distribution in the population using a number of approaches, such as cataloguing its frequency in different populations, examining environmental factors that exacerbate or ameliorate its effects and assessing its origins and its typical effect on the time course of, for example, disease expression among individuals.

By integrating data from multiple high‐throughput biomedical assays (e.g. data from epigenomics, metabolomics, proteomics and metabolomics), genetic epidemiologists can apply ‘system‐level’ approaches to understand how various factors contribute to interaction in the expression of health‐related traits and diseases.
Genetic Risk: Computation
Authors: Grimm Tiemo , Müller‐Myhsok Bertram , Zerres Klaus 
Published: October 2017

AbstractDespite the progress of molecular genetics and the resulting improved possibilities for precise risk classification in affected families, the principles of formal risk assessment continue to be of great importance as a decision‐making aid for a targeted molecular genetic analysis and an adequate interpretation of molecular findings. Assuming a genetic model, which is both the basis for risk assessment and the interpretation of molecular findings is of great importance. Even in the molecular era Bayesian theorem has to be applied in monogenetic diseases like Huntington disease, spinal muscular atrophy and Duchenne muscular dystrophy. Precise risk assessment in genetic counseling often deserves Bayesian risk calculation.Key ConceptsRisk assessment in families with genetic diseases is of great importance in spite of improved molecular diagnostics.Risk assessment is important for both the indication of molecular diagnostics and the interpretation of possible molecular findings.The prerequisite for the risk assessment is the assumption of a specific genetic model.Taking a larger number of variables (e.g. incomplete penetrance, spontaneous mutations and late onset) into account, risk calculation can significantly modify a priori risks.
Zebrafish as a Model for Human Diseases
Authors: Tavakoli Sahar , Rothschild Harriet , Zon Leonard I 
Published: October 2017

Abstract

The zebrafish, Danio rerio (a tropical and small freshwater fish), is an early vertebrate model organism. Its use in modelling human disease has numerous advantages over other animals as zebrafish have a fully sequenced genome, high fecundity, short generation interval (3–4 months), rapid embryonic development, external fertilisation and translucent embryos. External fertilisation and transparent zebrafish embryos allow for gene function studies at the early stages of the embryogenesis, for access to all stages of development and for time‐lapse imaging of progressing pathologies. In addition, zebrafish are economically viable for large‐scale genetic and chemical screens, which is not feasible in other vertebrate model organisms. Advances in the techniques and coincidentally these characteristics of zebrafish confer an advantage over murine biology and therefore elevate zebrafish as a critical human disease model and research tool.

Key Concepts

The zebrafish, Danio rerio, is a small tropical freshwater fish that belongs to the Cyprinidae family of the order Cypriniformes.

A model organism is any nonhuman organism which is widely used to study and understand biological processes in order to provide a better understanding of disease processes in human disease research.

Because of its external fertilization, high fecundity, translucent embryos, short generation interval, rapid embryonic development, fully sequenced genome and similar genome to humans, the zebrafish became a useful animal model to study human diseases.

Genetic screens are used to identify new genomic regions that contribute to a particular phenotype within a population of genetically mutagenised individuals. This laboratory procedure provides a useful platform to study gene function.

Transplanting donor zebrafish tissue into a recipient is a useful tool to study cell engraftment and tumour metastasis in a uniform background.
Atherosclerosis: Pathogenesis, Genetics and Experimental Models
Authors: Mota Roberto , Homeister Jonathon W , Willis Monte S , Bahnson Edward M 
Published: October 2017

Abstract

Atherosclerosis is a progressive disease of the arteries that results in the development of heart disease and stroke – the most common causes of death in developed countries and a growing socioeconomic burden in developing countries. Atherosclerosis results from an initial injury to the artery endothelium caused by mechanical and environmental factors, resulting in an inflammatory response in the vessel wall. The location and morphology of the atherosclerotic lesions predict the nature of the resulting vascular disease. Many risk factors for the disease are well known, and current therapies are largely directed at modifying them; however, the large array of poorly understood polygenetic factors affects the development of atherosclerosis. 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 for which recent studies in the field extend such hypothesis towards the degree of the inflammatory response to such injury.

Atherosclerotic lesions in humans have distinctive morphological characteristics and complications that differ in current animal models, the clinical manifestations correlate mostly 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 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.

Rodent models such as APOE‐ and LDLR‐deficient mice are widely used to study the pathogenesis of atherosclerosis because of its reproducibility and genetic manipulation; however, recent studies with novel and bigger animal models more accurately resemble human disease.
Pathological Mutations in 5′ Untranslated Regions of Human Genes
Authors: Chatterjee Sangeeta , Rao Shilpa J , Pal Jayanta K 
Published: October 2017

Abstract

The 5′ untranslated region (5′‐UTR) of a messenger ribonucleic acid (mRNA) plays a critical role in translational regulation by influencing mRNA stability and translation efficiency. Functional elements in the 5′‐UTR such as internal ribosome entry site (IRES), upstream open‐reading frames (uORFs) and iron‐responsive element (IRE) serve to fine tune protein expression in response to cellular requirement. Genetic variations such as mutations and single nucleotide polymorphisms (SNPs) in the 5′‐UTR are associated with a number of human diseases and increased susceptibility to diseases. Such pathological variations disrupt the motifs at the 5′‐UTR and cause diseases such as X‐linked Charcot‐Marie‐Tooth (CMTX) disease, multiple myeloma, hereditary hyperferritinaemia/cataract syndrome (HHCS), familial predisposition to melanoma, Marie Unna hereditary hypotrichosis (MUHH), oesophageal cancer and many others. Genetic and molecular profiling of many diseases has shown that a holistic approach including the UTRs in regular diagnostic deoxyribonucleic acid (DNA) screening would aid in better disease profiling and disease management.

Key Concepts

5′ Untranslated regions (UTRs) are noncoding regions of messenger ribonucleic acids (mRNAs).

The 5′‐UTR is delimited by transcriptional initiation site at 5′ end and the physiological start codon (AUG) at the 3′ end.

Motifs such as internal ribosome entry site (IRES), upstream open‐reading frames (uORFs), iron‐responsive element (IRE) and others are involved in mRNA stability and translational control.

mRNAs encoding regulatory proteins need to be strongly and precisely regulated. These mRNAs are often endowed with longer than average 5′‐UTR, uORFs and stable secondary structures that regulate their translation efficiency.

Mutations are changes in the DNA/genes of an organism, which are heritable.

Mutations that disrupt the functional elements of the 5′‐UTR are often associated with diseases.

Single nucleotide polymorphisms (SNPs) in the 5′‐UTR are associated with drug response and disease risk in an individual.
Neurogenomics of Behavioural Plasticity in Socioecological Contexts
Authors: Baker Matthew R , Hofmann Hans A , Wong Ryan Y 
Published: October 2017

Abstract

Social and ecological challenges often elicit behavioural and physiological responses that are adaptive and subject to selection. The varying behavioural states and traits of animals are a direct output of the nervous system and underlying molecular substrates. Changes in gene expression in response to a variety of contexts such as mate choice, aggression and developmental experience can alter a number of cellular and neural pathways that lead to changes in behaviour. A common framework has emerged to understand the role of the transcriptome in animal behaviour. Behavioural plasticity describes both an individual's ability to modify behavioural states and correlated suites of behaviour in populations, which may constrain variance across contexts. By integrating the study of behavioural plasticity with genome scale, bioinformatics and candidate gene analyses, we are rapidly expanding our understanding of this kind of organismal flexibility, its relationship with the genome and its evolutionary implications.

Key Concepts

To understand animal behaviour fully, both the proximate (causation and ontogeny) and the ultimate (function and evolution) mechanisms of behaviour must be considered and integrated.

Utilising both forward and reverse genetics, candidate genes underlying a behaviour can be better identified and characterised.

The genome is plastic and flexible in response to social or environmental cues, which can lead to changes in behaviour.

Comparative transcriptomics across species can help identify and characterise conserved mechanisms of animal behaviour.

The relationship between behavioural evolution and the processes that generate structural variation in the genome is not well understood and needs to be considered.

The proposed framework will streamline future studies to uncover not only the genetic and neural mechanisms of complex animal behaviours but also its adaptive function and evolution.