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Disaster Risk Management: Disciplinary status and prospects for a unifying theory

Disaster Risk Management: Disciplinary status and prospects for a unifying theory

As a result a unique field of study may emerge – typically as a branch from one of the established disciplines. Should there be adequate impetus and interest in the field – usually stimulated by needs of industry – a distinctive corpus of knowledge emerges (Nachmias & Nachmias 1976:4). Therefore, over time, a field or branch of study may progress through various maturity levels to become a new entrenched discipline. Maturation of an independent academic discipline is a time-consuming process, in which a field of study acquires the status of a formal discipline, step by step. A field of study can be regarded as ‘matured’ if it relies on its own unifying theory and knowledge base (Lowenstein 2004:30). Theorists usually simply differentiate between well- established (mature) disciplines that have a long history with a well-established set of theories and approaches, and new emerging fields – supported by only a few universities and publications. An incremental maturity process is usually evident where knowledge production regarding a certain phenomenon gradually evolves to accommodate best practices, theories, models, and approaches associated with more mature, related disciplines.
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The origin of allometric scaling laws in biology from genomes to ecosystems: towards a quantitative unifying theory of biological structure and organization

The origin of allometric scaling laws in biology from genomes to ecosystems: towards a quantitative unifying theory of biological structure and organization

Since our original paper was published (West et al., 1997), there have been several criticisms (Darveau et al., 2002; Dodds et al., 2001; White and Seymour, 2003). Some of these revolve around matters of fact and interpretation that still need to be resolved – such as the scaling of maximal metabolic rates in mammals or the precise value of the exponent. Others claim to provide empirical information or theoretical calculations that refute our models. We have not found any of these latter criticisms convincing for two reasons. First, most of them rest on single technical issues, for which there are at least equally supportable alternative explanations, and some that are simply incorrect. Furthermore, most of these have been concerned solely with mammalian metabolic rate, so they fail to appreciate that our theory offers a single parsimonious explanation, rooted in basic principles of biology, physics and geometry, for an enormous variety of empirical scaling relations. None of the criticisms offer alternative models for the complete design of vascular networks or for the M b 3/4
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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

In this chapter, I have tried to indicate some aspects of disease causation observable from the standpoint of a clinician, yet little considered to date by medical science, and with so little influence on the current philosophical of our approach to understanding disease causation. I hope to have persuaded the reader that a dynamic evolution of disease through a series of changing patho- physiological mechanisms over time is worthy of consideration, and that the general guidelines for theory formulation in medicine can be useful in developing models for understanding disease. In the final analysis, as much as it has tried to put forward new concepts on disease, this monograph has been concerned with finding new ways of seeing so that we might formulate concepts and models about it, particularly in areas where current theories are clearly deficient. If I have achieved some small advance in that respect, I shall be content.
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Hyperinsulinemia: A unifying theory of chronic disease?

Hyperinsulinemia: A unifying theory of chronic disease?

Hyperinsulinemia affects the body via five main mechanisms: Increased reactive oxidative species and advanced glycation end-products; increased insulin-like growth factor-1[r]

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Errata: Hyperinsulinemia: A unifying theory of chronic disease?

Errata: Hyperinsulinemia: A unifying theory of chronic disease?

Hyperinsulinemia affects the body via five main mechanisms: Increased reactive oxidative species and advanced glycation end-products; increased insulin-like growth factor-1[r]

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A unifying theory and improvements for existing approaches to text compression

A unifying theory and improvements for existing approaches to text compression

An algorithm is given which uses a binary search tree to fmd the longest string match, and experiments show that this results in a dramatic increase in encoding speed.... "There is nothi[r]

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Sparse modeling: some unifying theory and word-imaging

Sparse modeling: some unifying theory and word-imaging

• Chosen predictor words form a set known as the Word Image for q. • Word image must be evaluated two ways:[r]

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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

Such a theory could account for a great deal of the behavior of repetitive DNA in general. The existence of the various sequences of repetitive DNA in multiple copy number could now be related to the recurrence of viral infection with each new host generation over the long evolutionary time- period the virus remained in an infective relationship with the host species. Differences in repetitive DNA location from one individual to another among a species could be explained by the occurrence of different viral integration sites with each new host-infection. In addition, variability of repetitive DNA, including satellite consensus sequence type, might well be due to molecular evolution within the virus itself, and as such it would not be surprising if, being determined by selective mechanisms, it were of a non-random nature. On the other hand, the absence of particular repeat sequences from one of a group of related species could now be explained by the failure of a particular virus to interact with the species concerned, either because of the lack of an appropriate receptor for the virus, or because that species was not exposed to the virus by virtue of its being located in some different geographic ecosphere distribution. Occasionally, the absent sequences might have been deleted by homologous recombination via direct repeats at the ends of some satellite sequence block. This might occur, for example, when two insertion sequences, known to exist in at least some satellites, 37 happened to become incorporated into satellite DNA in such a way as to flank a stretch of its
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Development of a Unifying Theory for Data Mining Using Clustering Techniques

Development of a Unifying Theory for Data Mining Using Clustering Techniques

Cluster is a generally excellent way for ordering homogenous gatherings of articles called groups. Articles or perceptions that are indistinguishable will in general offer num[r]

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A Unifying Theory for the Litigation of Computer Software Copyright Cases, 6 Computer L.J. 55 (1985)

A Unifying Theory for the Litigation of Computer Software Copyright Cases, 6 Computer L.J. 55 (1985)

In Diehr the only novel aspect also was the improvement in the speed of calculating a well-known equation in a standard industrial process. Arguably, the only distinctio[r]

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Unus pro omnibus, omnes pro uno: A novel, evidence-based, unifying theory for the pathogenesis of endometriosis

Unus pro omnibus, omnes pro uno: A novel, evidence-based, unifying theory for the pathogenesis of endometriosis

The theory of retrograde menstruation as aetiopathogenesis of endometriosis formulated by John A Sampson in 1927, shows clear shortcomings: this does not explain why retrograde menstruation is a physiological process that affects 90 % of women, while endometriosis occurs in only 10 % of cases; it also does not explain the endometriotic foci distant from the pelvis, nor explains the cases of endometriosis in male patients. The immunological alterations of the peritoneal fluid explains the effects of disease, such as the inhibition of the physiological processes of cytolysis, but does not explain the cause. There is evidence to support the hypothesis that müllerian remnants of the endometrium, and endocervix endosalpinx, ectopic, are items from the genital ridge leaked during organogenesis. It is known that tissues derived from coelomatic epithelial and mesenchymal cells have the potential to metaplastically differentiate into epithelium and stroma. In addition, the phenotype of the ectopic endometrial cells is significantly different from those eutopics. There is no scientific evidence that, during organogenesis, the genes of the Homeobox and Wingless family play a fundamental role in the differentiation of the ducts of Muller and development of the anatomical structure of the urogenital tract. We present here a hypothesis that deregulation of genes and the Wnt signaling pathway Wnt/ β-catenin leads to aberrations and deregulation within the mesoderm, thus, may cause aberrant placement of stem cells. In addition, immune cells, adhesion molecules, extracellular matrix metalloptroeinases and pro- inflammatory cytokines activate/alter cells, creating the conditions for differentiation, adhesion, proliferation and survival of ectopic endometrial cells.
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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

The first assumption, it will be recalled, is that population size remains relatively finite and estimable. The trouble is that this results in a calculated population size that is often far too small to account for the observed speed of evolution, particularly that occurring at the molecular level. But with the sort of viral/host interchange relationship envisaged under the present theory, the genetic pool with which any population or species was in contact at any one time would be enormously increased. Even a single cell infected with a number of integration viruses during its life-time might be exposed in this way to millions of viral genetic particles, each having at least some potential to insert at different points within the host genome, and each perhaps carrying differently evolved viral variants, as well as different host-gene fragments around its site of incorporation due to imprecise excision from some previous host. Add to this the broad range of viruses that may infect any one host species, as well as the potential for genetic contact between different species through the overlapping virus/host
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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

Aetiological Diagnosis Having gained some idea of the general diagnosis, we next have to delve into the background and ask, “Why did this particular patient get this condition?” This is [r]

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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

fortunately for them, other molecular data began to arise in its support. Particularly important was the finding of a widespread heterozygosity within populations — i.e. the occurrence of a different gene variant at each of the two genetic loci present within each chromosome pair of any one individual — and this was found not only within the odd species here and there, but over a wide variety of them. 34 It was one thing to accept some sort of diversifying natural selection as an explanation of such different gene variants between populations of species separated by wide geographic distances (i.e. polymorphism), but quite another to account for any extensive heterozygosity within the individuals among those populations. According to classical selection theory, the gene pool of any population in equilibrium with its environment should be homozygous for the adaptive gene at virtually every locus, and heterozygous for mutant alleles only at a very small number of genetic sites 12 But electrophoretic mobility studies showed a protein
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Towards a unifying theory of generalization

Towards a unifying theory of generalization

Gaussian Process regression provides a useful tool to address all of these questions. First, as different forms of generalization can be encoded directly into Gaussian Process regres- sion models, and as these forms can also be combined explicitly (Duvenaud et al., 2013), it can be used to derive a compositional theory of functions in which smaller parts are com- bined to explain complex structural patterns. Second, as Gaussian Process regression is also a common tool for problems involving the optimization of unknown functions (Snoek et al., 2012), it is an informative method to assess how humans approach tasks incorporat- ing both function learning and the search for rewards. Third, as a mechanism of general- ization can theoretically be applied to many other psychological domains, from learning causal relata from observations (Hoyer et al., 2009) to inferring people’s intentions from their actions (Wang et al., 2012), a final question will be how much a theory of generaliza- tion grounded in function learning itself generalizes to other tasks, i.e. in what sense the proposed model can indeed be seen as a universal law, a psychological process model, or just a window into an empirically observed phenomenon.
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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

beyond, it still tries to keep within the bounds of the reasonable by drawing on such tangible supports as models and analogies borrowed from other fields of experience. Although the data tackled are often difficult, the basic approach remains in essence simple, and certainly no deep philosophical models are involved. Indeed, the approach facilitates the further drawing together of common basic overall threads at the end of the book to allow me to put forward a unified theory linking stress, disease, and evolution. The book ends by returning again to its central theme, namely how we might proceed to achieve a better understanding of disease mechanisms within the always-limited frameworks of existing data.
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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

there is not complete agreement between the result of one‟s work and experiment, one should not allow oneself to be too discouraged, because the discrepancy may well be due to minor features that are not properly taken into account, and that will get cleared up with further developments of the theory”. By so saying (about Schroedinger‟s initial hesitations), Dirac clearly indicates that if a hypothesis has aesthetic appeal, one should not let it be destroyed too easily by the odd discordant experimental fact! This view is also clearly apparent in many of the writings of others who have made discoveries in science. It should not, in fact, cause great surprise or concern, for it is a view widely espoused when supporting traditional or established theories. New theories are only ever likely to be accepted if they explain a substantially greater body of evidence than the old. Of course, one cannot carry this view too far in support either of new or old theories. But to say that traditional theories cannot become propped up far beyond their basis in the evidence would be to deny that Kuhn 4 is at least occasionally right when he says that something like a revolution is sometimes required to supplant an outmoded tradition by a new one.
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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

alternative explanation. It is difficult, along the lines of the present vasospastic theory, to see how monoclonality could arise where arterial wall damage was severe enough to involve the media, as it frequently does in experimental atherosclerosic lesions. 8 There, the smooth muscle cells involved seem to migrate from the medial layer to the intima, 61 and in numbers far too large to support a monoclonal basis for any subsequent atherosclerotic plaque. But judged from the early fatty streaks, grey gelatinous intimal elevations etc. in the young 16 , damage in the human disease may be much more superficial, and this may mean that it is only the smooth muscle cells of the intima itself which are provoked to proliferate. Now, the "myo-intimal" cell is very sparsely distributed in the intima, at least in the newborn, 8 so that local damage from constriction at any one point might initially stimulate only one such cell in early childhood, from which monoclonal origin the plaque could gradually evolve over the years, through repeated bouts of endothelial damage and its consequences.
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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

neoplasia, and second that such a theoretical view is sufficiently well supported by existing evidence to encourage to encourage pursuing it further. Yet, for the moment, I do not wish to do this because, for one thing, we just do not yet have enough evidence on which to evaluate it fully. More importantly, such a theory would so strongly challenge the whole basis of our whole understanding of the evolution of the genome, that it is in this light in which it must first be examined. Such analysis will be the subject of the next chapter, but before that, I want to explain that reflections on the possible origins of carcinoma were not my only reasons for developing this viral view of evolution because, quite independently, I had been drawn to similar conclusions through an analogy I developed to explain a separate and quite serious problem with evolutionary theory itself. Again, the details of that evolutionary problem will be discussed more fully later, and I will give here only sufficient synopsis of its outline to set the stage both for illustrating the analogy itself, and for showing how it might help to understand the
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On Stress Disease and Evolution: A Unifying Theory

On Stress Disease and Evolution: A Unifying Theory

In these days of biochemical reductionism as an approach to understanding disease, what was once thought to be a clear-cut psychosomatic basis for this and many other diseases 51,55 now seems to have faded somewhat into the background. Nonetheless, duodenal ulcer is still acknowledged by many as a fairly classical psychosomatic condition, and there is evidence to support this. 56 Psychosocial situations which lead to the general feeling of being deprived of one‟s just due appear to be particularly important in precipitating ulcer pain and discomfort in many patients, 51,56 and it is of interest that the similar moods of dejection, despair etc. have been noted by Wolff to cause pallor and ischaemia of the gastrointestinal mucosa. 11 Clinically, so-called „chronic‟ duodenal ulcer characteristically runs a periodic course with relapses and remissions presumably corresponding to recurrent episodes of breakdown and healing of the mucosa in the proximal duodenum, so that it certainly qualifies as an acute reversible stress-related condition for consideration under the present theory.
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