网范文：“Evolutionary information dynamics of cancer ” 种族之间的差距,尤其是在疾病方面比较凸显，例如乳腺癌和前列腺癌。这篇社会范文讲述了对于癌症的演变和进展情况。对美国而言,奴隶制及其后遗症，黑人和白人,明显对比疾病患病率，社会经济地位和生活方式的调整,而统计占大部分的方差在乳腺癌,最终只有回避了问题的因果关系。这里提出一个更基本的生物学解释，对于免疫认知理论包括一个复杂的肿瘤控制机制。
它们之间的相互影响发生在一个嵌入的背景下,高度结构化的、系统的社会心理压力。在疾病过程中,加速突变率,和抑郁的突变控制。动力学是类似于简单的进化系统间断平衡。下面的范文进行详述。
Abstract
‘Racial’ disparities among cancers, particularly of the breast and prostate, are something of a mystery. For the US, in the face of slavery and its sequelae, centuries of interbreeding has greatly leavened genetic differences between ‘Blacks’ and ‘whites’, but marked contrasts in disease prevalence and progression persist. ‘Adjustment’ for socioeconomic status and lifestyle, while statistically accounting for much of the variance in breast cancer, only begs the question of ultimate causality. Here we propose a more basic biological explanation thatextends the theory of immune cognition to include an elaborate tumor control mechanism constituting the principal selection pressure acting on pathologically mutating cell clones.
The interplay between them occurs in the context of an embedding, highly structured, system of culturally-specific psychosocial stress. A Rate Distortion argument finds that larger system able to literally write an image of itself onto the disease process, in terms of enhanced ‘risk behavior’, accelerated mutation rate, and depressed mutation control. The dynamics are analogous to punctuated equilibrium in simple evolutionary systems, accounting for the staged nature of disease progression. We conclude that ‘social exposures’ are, for human populations, far more than incidental cofactors in cancer etiology. Rather, they are part of the ‘basic biology’ of the disorder. The aphorism that ‘culture is as much a part of human biology as the enamel on our teeth’ appears literally true at a fundamental cellular level.
KEY WORDS: Cancer, cellular cognition, culture, evolution, information theory, interpenetration, mutator, punctuation
Introduction
Cardiovascular disease and cancer are major causes of mortality in the United States structured by ‘race’, class, and gender [28]. Cancers of the breast and prostate - ‘hormonal’ cancers - particularly show large disparities by ethnicity and economic class in incidence among young adults, stage at presentation, and mortality rate (e.g. [39]). Although certain genetic alleles predispose individuals to higher susceptibility for these cancers (e.g. [23] for prostate cancer), recent changes of incidence and mortality in time and geography indicate genes alone do not explain the expressed population-level patterns.
At present, African-American women under age 35 suffer an approximately two-fold higher age-specific rate of breast cancer, compared to white women, and the mortality rate is about three times higher [44]. For prostate cancer, African-American men have a 2-fold higher mortality rate, and 50 percent higher incidence rate, than their white counterparts [43]. During the 1980’s, when ideologies of individualism particularly influenced US scientific thinking, interest in health differentials waned. In its stead, the life style doctrine arose: people get sick because they don’t takeresponsibility for their own health.
The connection between diet and breast cancer was an often-cited example of how life style affects health. By the 1990’s, however, a large literature on determinants of risk behaviors explored the bases of ‘life style’ decisions and found them rooted in social and economic processes (e.g. [11, 22, 30, 58, 59]). Many of the risk behaviors associated with AIDS, drug abuse, and violence, were shown to be coping mechanisms for dealing with frustration, pain, deprivation, humiliation, and danger (e.g. [7, 58, 59]). The particular modes of coping spread, first between social networks and then within social networks by branching processes [32]. Indeed, one of the classic studies of drug use, The Heroin Epidemics, described all these contagious small-scale processes early on [29]. Risk behaviors may explain part of the pattern in hormonal cancers.
Such behaviors, however, may not totally explain population differentials in hormonal cancer incidences and mortality rates. We propose an approach that more fully integrates the biocultural processes that shape the development of humans, their cancers, and differentials in both their susceptibility and pathways of disease progression. We begin with Nunney’s [37] evolutionary history of cancer, as opposed to more conventional local evolutionary dynamic theories of tumorigenesis within an organism (e.g. [8]). Nunney’s analysis suggests that in larger animals, whose lifespans are proportional to about the 4/10 power of their cell count, prevention of cancer in rapidly proliferating tissues becomes more difficult in proportion to their size. Cancer control requires the development of additional mechanisms and systems to address tumorigenesis as body size increases – a synergistic effect of cell number and organism longevity.
Nunney’s work implies, in particular, that different tissues may have evolved markedly different tumor control strategies. All of these, however, are likely to be energetically expensive, permeated with different complex signaling strategies, and subject to a multiplicity of reactions to signals.
For modern humans, large animals whose principal selective environment is otherhumans, this suggests a critical role for the ‘signal’ of psychosocial stress, as mediated by a local ‘sociocultural network’, i.e. an embedding cognitive social structure linked to a cultural practice and history. Contemporary evolutionary anthropology (e.g. [18]) emphasizes that culture, largely defining what social relations are particularly helpful or stressful, has become inextricably intertwined with human biology. Recent analysis (e.g. [21]) suggests that psychosocial stress is a very strong signal indeed and severally affects the stages of mutation control: immune surveillance, both DNA damage and repair, apoptosis, and rates of somatic mutation – the ‘mutator phenotype’ we will explore at length below.
Review of formalism
Before beginning the formal treatment, we highlight several important points: First, information theory is notorious for providing ‘existence theorems’ whose application is arduous indeed. For example, while the Shannon Coding Theorem implied the possibility of very efficient coding schemes as early as 1949, it took more than forty years for practical ‘turbo codes’ to be created. Our adaptation of the Shannon Source Coding Theorem is unlikely to be less difficult. Second, we are invoking information theory variants of the fundamental asymptotic limit theorems of probability. These are independent of exact mechanism, but constrain the collective behavior of such mechanisms.
For example, although not all processes involve long sums of individual stochastic variables, those that do, regardless of the individual variable distributions, follow a Normal distribution as a consequence of the Central Limit Theorem. Similarly, the games of chance in a Las Vegas casino are all quite different, but nonetheless the possible success of ‘strategies’ for playing themis strongly and systematically constrained by the Martingale Theorem, regardless of game details.
We similarly propose that languages-on-networks and languages-that-interact, as a consequence of the limit theorems of information theory, will be subject to regularities of punctuation and ‘generalized Onsager relations’, regardless of detailed mechanism, as important as the latter may be. Finally, just as we often impose parametric statistics on sometimes questionable experimental situations, relying on the robustness of the Central Limit Theorem to carry us through, we will invoke a similar heuristic approach in our applications of the information theory limit theorems.
Discussion and conclusions
We have applied an elaborate mathematical modeling strategy to the problem of disparities in occurrence and progression of certain cancers between powerful and marginal subgroups. As the ecologist E.C. Pielou has argued [40, p. 106], a severe methodological limit to any such approach is that mathematical models do not create new knowledge, they create new speculation, even when they appear to fit available data quite well. Their often considerable utility lies almost entirely in raising questions for subsequent empirical study, which, in a scientific context, is the only true source of new knowledge. The speculations emerging from our model are of some interest. We have expressed tumorigenesis in terms of a synergistic linkage of a ‘language’ of structured external stress with the adaptive mutator and its opposing cognitive process, mutation control. Raised rates of cellular mutation which quite literally reflect biocultural selection pressure through Ademi’s distorted mirror do not fit a cognitive paradigm: The adaptive mutator may propose, but selection disposes.
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