Home About us Contact
|
Home About us Contact | ||
|
|
||
Comprehensive Explanation (comprehensive + explanation)
Selected AbstractsTHE INTERACTION OF ANTISOCIAL PROPENSITY AND LIFE-COURSE VARYING PREDICTORS OF DELINQUENT BEHAVIOR: DIFFERENCES BY METHOD OF ESTIMATION AND IMPLICATIONS FOR THEORY,CRIMINOLOGY, Issue 2 2007GRAHAM C. OUSEY Recent criminological research has explored the extent to which stable propensity and life-course perspectives may be integrated to provide a more comprehensive explanation of variation in individual criminal offending. One line of these integrative efforts focuses on the ways that stable individual characteristics may interact with, or modify, the effects of life-course varying social factors. Given their consistency with the long-standing view that person,environment interactions contribute to variation in human social behavior, these theoretical integration attempts have great intuitive appeal. However, a review of past criminological research suggests that conceptual and empirical complexities have, so far, somewhat dampened the development of a coherent theoretical understanding of the nature of interaction effects between stable individual antisocial propensity and time-varying social variables. In this study, we outline and empirically assess several of the sometimes conflicting hypotheses regarding the ways that antisocial propensity moderates the influence of time-varying social factors on delinquent offending. Unlike some prior studies, however, we explicitly measure the interactive effects of stable antisocial propensity and time-varying measures of selected social variables on changes in delinquent offending. In addition, drawing on recent research that suggests that the relative ubiquity of interaction effects in past studies may be partly from the poorly suited application of linear statistical models to delinquency data, we alternatively test our interaction hypotheses using least-squares and tobit estimation frameworks. Our findings suggest that method of estimation matters, with interaction effects appearing readily in the former but not in the latter. The implications of these findings for future conceptual and empirical work on stable propensity/time-varying social variable interaction effects are discussed. [source] Patterns in naevoid skin disease: development, disease and modellingEXPERIMENTAL DERMATOLOGY, Issue 3 2010Stephen J. Gilmore Please cite this paper as: Patterns in naevoid skin disease: development, disease and modelling. Experimental Dermatology 2010; 19: 240,245. Abstract:, The aetiology of pattern-formation in human naevoid skin disease remains unknown. However, it is likely that the majority of previously proposed mechanisms , those that simply rely on passive clonal trafficking in embryogenesis , are incomplete. A more comprehensive explanation for pattern-formation in naevi invokes the principle of self-organization. We define two types of patterning: anatomical and functional. Anatomical patterning is where the abnormal clone is limited to regions of pathologic skin, while functional patterning is where the abnormal clone and pathologic skin are spatially uncorrelated. From a theoretical perspective self-organized naevoid patterns may be either secondary to local interactions between normal and aberrant genotypes or due to the interaction between aberrant genotypes and the presence of normal embryonic patterning cues. The latter possibility suggests the critical observation and analysis of patterns in naevoid skin disease may lead to unique insights into key aspects of early human embryogenesis. [source] Vapor,Solid,Solid Growth Mechanism Driven by Epitaxial Match between Solid AuZn Alloy Catalyst Particles and ZnO Nanowires at Low Temperatures,ADVANCED MATERIALS, Issue 8 2008Leonardo C. Campos A comprehensive explanation for the precise mechanism of ZnO nanowire growth at low temperatures (T,<,400,°C) is presented. Experimental data and theoretical considerations evidence that ZnO nanowires originate from solid ,-AuZn catalyst particles. A model is proposed to describe such growth. An original feature of the model concerns the formation of nanowire, which occurs via preferential oxidation of specific ,-AuZn surfaces induced by epitaxial-like growth mechanism. [source] MIT Roundtable on Corporate Risk ManagementJOURNAL OF APPLIED CORPORATE FINANCE, Issue 4 2008Article first published online: 16 DEC 200 Against the backdrop of financial crisis, a distinguished group of academics and practitioners discusses the contribution of financial management and innovation to corporate growth and value, along with the pitfalls and unintended consequences of such innovation. The main focus of most panelists is the importance of a capital structure and risk management approach that complement the strategy and operations of the business. Instructive examples are provided by Judy Lewent, former CFO and head of strategic planning at Merck, and Lakshmi Shyam-Sunder, director of finance and risk management at the International Finance Corporation. But if these represent successful applications of finance theory, what about the large number of cases where the use of derivatives and other innovations has led to high leverage and apparent risk management failures? Part of the current trouble, as pointed out by Andrew Lo, can be attributed to the failure of risk managers and their models to account for highly improbable events,the so-called fat tails of the distribution. But, as Robert Merton suggests in closing, there is a more comprehensive explanation for today's problems: the tendency of market participants to respond to potentially risk-reducing financial innovation by increasing their risk-taking in other areas. "What we have here," says Merton, ,are two partly offsetting effects of innovation,one that is reducing the risk of companies and their investors, and another that is encouraging greater risk-taking. From a social or regulatory standpoint, the goal is to find the right balance between these two effects or forces. [source] When Thailand was an island , the phylogeny and biogeography of mite harvestmen (Opiliones, Cyphophthalmi, Stylocellidae) in Southeast AsiaJOURNAL OF BIOGEOGRAPHY, Issue 6 2010Ronald M. Clouse Abstract Aim, To develop a comprehensive explanation for the biological diversity of Southeast Asia, especially in the Wallacea and Sundaland regions. This study focuses on a group of arachnids, mite harvestmen, which are thought to be an extremely old group of endemic animals that have been present in the region since most of its land supposedly formed part of the northern rim of the supercontinent Gondwana. Location, Eastern Himalayas, Thai-Malay Peninsula, Sumatra, Borneo, Java, Sulawesi, and New Guinea. Methods Approximately 5.6 kb of sequence data were obtained from 110 South-east Asian Cyphophthalmi specimens. Phylogenetic analyses were conducted under a variety of methods and analytical parameters, and the optimal tree was dated using calibration points derived from fossil data. Event based and paralogy-free subtree biogeographical analyses were conducted. Results, The Southeast Asian family Stylocellidae was recovered as monophyletic, arising on what is now the Thai-Malay Peninsula and diversifying into three main clades. One clade (Meghalaya, here formally placed in Stylocellidae) expanded north as far as the eastern Himalayas, a second clade entered Borneo and later expanded back across the Sundaland Peninsula to Sumatra, and a third clade expanded out of Borneo into the entire lower part of Sundaland. Molecular dating suggested that Stylocellidae separated from other Cyphophthalmi 295 Ma and began diversifying 258 Ma, and the lineage that inhabits mostly Borneo today began diversifying between 175 and 150 Ma. Main conclusions, The topology and molecular dating of our phylogenetic hypothesis suggest that Stylocellidae originated on Gondwana, arrived in Southeast Asia via the Cimmerian palaeocontinent, and subsequently diversified north, then south. Their present distribution in the Indo-Malay Archipelago is explained largely by a diversification over the Sundaland Peninsula before western Sulawesi departed and the peninsula was extensively inundated. [source] War-related posttraumatic stress disorder in Black, Hispanic, and majority White Vietnam veterans: The roles of exposure and vulnerabilityJOURNAL OF TRAUMATIC STRESS, Issue 2 2008Bruce P. Dohrenwend Elevated prevalence rates of chronic posttraumatic stress disorder (PTSD) have been reported for Black and Hispanic Vietnam veterans. There has been no comprehensive explanation of these group differences. Moreover, previous research has relied on retrospective reports of war-zone stress and on PTSD assessments that fail to distinguish between prevalence and incidence. These limitations are addressed by use of record-based exposure measures and clinical diagnoses of a subsample of veterans from the National Vietnam Veterans Readjustment Study (NVVRS). Compared with Majority White, the Black elevation is explained by Blacks' greater exposure; the Hispanic elevation, by Hispanics' greater exposure, younger age, lesser education, and lower Armed Forces Qualification Test scores. The PTSD elevation in Hispanics versus Blacks is accounted for mainly by Hispanics' younger age. [source] Involvement of apoptosis and cholinergic dysfunction in Alzheimer's diseasePSYCHOGERIATRICS, Issue 2006Shinji TAGAMI Abstract As Alzheimer's disease (AD) progresses, brain atrophy becomes conspicuous, and histologically there is neuronal loss, primarily with a deficit of cholinergic neurons observed. Hitherto, the view has been that cell death, apoptosis, plays a role in this neuronal loss. Apoptosis is characterized by the morphological changes of nuclear fragmentation, chromatin condensation and cell shrinkage, with activation of caspases, members of the cysteine protease family, resulting in considerable substrate cleavage. TUNEL positive neurons have in fact been detected in AD brain, indicating increased caspase activity and resulting substrate cleavage. In AD brain, amyloid beta peptides (A,), the main constituent of senile plaque, are a specific pathological hallmark observed in extracellular spaces. In contrast, the main constituent of intracellularly observed neurofibrillary tangles (NFT) is hyperphosphorylated tau, which is observed in various neurodegenerative disorders other than AD. The viewpoint of many studies is that the A, and NFT that cause these neuropathological changes probably participate in neuronal death. However, up until now it has been thought that there was no hypothesis offering a comprehensive explanation of how the accumulation of extracellular A, and intracellular NFT leads to neuronal death. This report first covers the mechanism of apoptosis as clarified by molecular biological methods, and provides an explanation of how apoptosis could be involved in AD pathology. The subject of autophagic cell death, a type of cell death morphology that has recently been the focus of attention, is also addressed. [source] | ||||||||||