网范文：“Immune cognition, social justice and asthma” 这篇医学范文的目的是研讨红外免疫工作的作用，认知了解哮喘的发病率和死亡率。范文的探讨措施是通过免疫认知与中枢神经系统结合，通过他们与人接触应对的问题。使用一个数学模型,我们发现外部强加的结构性压力的模式,通过他们作用孩子的社交文化,成为协同免疫认知的发展方向,哮喘和其他免疫疾病的前兆。
在美国自1980年以来哮喘的发病率和死亡率已经上涨了近50%。1994年与哮喘有关的医疗病人占六分之一的急诊科。到1994年,近15%的城市孩子都患有哮喘,总体来说，英语论文题目，占整个美国人口的7%。下面的范文进行详述。
ABSTRACT
Objective: We explore the implications of IR Cohen’s work on immune cognition for understanding rising rates of asthma morbidity and mortality in the US. Methods: Immune cognition is conjoined with central nervous system cognition, and with the cognitive function of the embedding sociocultural networks by which individuals are acculturated and through which they work with others to meet challenges of threat and opportunity. Using a mathematical model, we find that externally-imposed patterns of ‘structured stress’ can, through their effect on a child’s socioculture, become synergistic with the development of immune cognition, triggering the persistence of an atopic Th2 phenotype, a necessary precursor to asthma and other immune disease. Conclusions: Reversal of the rising tide of asthma and related chronic diseases in the US thus seems unlikely without a 21st Century version of the earlier Great Urban Reforms which ended the scourge of infectious diseases.
Key words: American Apartheid, asthma, atopy, immune cognition, information theory, large deviation theory, renormalization, stress.
Introduction
Morbidity and mortality from asthma have risen nearly 50 % in the US since 1980 [1, 2]. In 1994 asthma-related demand for medical care accounted for one sixth of all emergency room visits and one out of eleven doctors’ office visits [2]. By 1994, nearly 15 % of all urban children were afflicted with asthma, compared with 7 % of the entire US population. Among children one to four years of age, asthma hospital discharge rates increased 57 % between 1980 and 1992, nationally, and African-American children in this age range were six times more likely to die of asthma than Caucasian children [1].
Carr et al. [3] described the late 1980’s geography of asthma in New York City: Minority neighborhoods such as Harlem, the South Bronx, BedfordStuyvesant, North Crown Heights and Washington Heights showed roughly five times the asthma mortality incidence of that found in affluent neighborhoods such as the Upper East Side, South Staten Island, and Forest Hills. Carr et al. [3] found that “Household income, percentage of population Black, and percentage of population Hispanic were significant predictors of area hospitalization rates (adjusted R2 = 0.75).” This pattern, which was later confirmed by DePalo et al. [4], is typical for other large US cities as well [5, 6], and suggests, prima face, that the highly structured psychosocial stressors of the system of American Apartheid have very recently become entrained into the developing immune systems of urban minority children. We explore mechanisms by which such a ‘phase transition’ can take place, and, at the population level, produce widespread precursor conditions for a subsequent outbreaks of asthma and related atopic diseases. Asthma is necessarily associated with failure of the child’s developing immune system to switch from the Th2 ‘humoral’ phenotype thought necessary to prevent maternal rejection in utero to a predominantly Th1 ‘cellular’ phenotype more suited to the functioning of acquired immunity [7]. Biochemical feedback mechanisms tend to fix one or the other mode once it becomes developmentally predominant, although they tend to overlap somewhat, and are not ‘orthogonal’ [7]. This mechanism will be the focus of our modeling exercise.
Clearly, then, the gestational and neonatal environment of the developing immune system will be critical in the ‘decision’ as to whether Th1 or Th2 3 immune phenotypes will predominate. Wright et al. [9] put the essential hypothesis as follows: “Prospective seroepidemiological studies have shown that the newborn period is dominated by Th2 reactivity in response to allergens, and it is also evident that the Th1 memory cells selectively develop shortly after birth (at 3-6 months of age) and persist into adulthood in non-atopic subjects. For most children who become allergic or asthmatic, the polarization of their immune systems into an atopic phenotype probably occurs during early childhood. These findings have sparked off vigorous investigation into the potential influence of early life environmental risk factors for asthma and allergy on the maturation of the immune system, in the hopes of understanding which factors will potentate (or protect from) this polarization... Although there is no direct evidence for the influence of stress on Th phenotype differentiation in the developing immune system, there is evidence that parental s of life stress are associated with subsequent onset of wheezing in children between birth and one year. It has been speculated that stress triggers hormones in the early months of life which may influence Th2 cell predominance, perhaps through a direct influence of stress hormones on the production of cytokines that are thought to modulate the direction of differentiation.”
The spatiotemporal pattern of the asthma increases among US children, in its exact match with patterns of residential segregation and community disintegration, suggests, however, that ‘stress’ is itself very highly structured. In this we will invoke Irun Cohen’s theory of immune cognition to argue that the developing immune system interacts with, and is affected by, structured patterns of external stress through the intermediate medium of a local embedding – and cognitive – sociocultural network, of necessity including immediate family. Our development will further suggest that the internally coherent grammar and syntax, in a large sense, of that stress ‘signal’ are no less important than its ‘magnitude’.
This is not an entirely new vision of the world. Recently, interactions between the central nervous system (CNS) and the immune system, and between the genetic heritage and the immune system have become officially recognized and academically codified through journals with titles such as Neuroimmunology and Immunogenetics. Here we will argue that a cognitive socioculture – a social network embodying culture – in which individuals are embedded, and through which they are both acculturated and function to meet collective challenges of threat and opportunity, may interact strongly with individual immune function to produce a composite entity which might well be labeled an Immunocultural Condensation (ICC).
We first examine current visions of the interaction between genes and culture, and between the CNS and culture, and follow with a summary of Cohen’s view of immune cognition. Next we argue that immune cognition and cognitive socioculture can become fused into a composite entity – the ICC – and that this composite, in turn, can be profoundly influenced by embedding systems of highly structured psychosocial and socioeconomic stressors. In particular, we argue that the internal structure of the stress – its ‘grammar’ and ‘syntax’ – are important in defining the coupling with the ICC. The Appendix to this presents a detailed mathematical model of the ICC and its linkage with structured patterns of psychosocial or socioeconomic stress which is based on adapting renormalization techniques from statistical mechanics to information theory, in the spirit of the Large Deviations Program of applied probability. The necessity of such an approach will emerge from examination of IR Cohen’s theory of immune cognition.
Genes, cognition, and culture
Increasingly, biologists are roundly excoriating simple genetic reductionism which neglects the role of environment. Lewontin [10], for example, explains that genomes are not ‘blueprints,’ a favorite public relations metaphor, as genes do not ‘encode’ for phenotypes. Organisms are instead outgrowths of fluid, conditional interactions between genes and their environments, as well as developmental ‘noise.’ Organisms, in turn, shape their environments, generating what Lewontin terms a triple helix of cause and effect. Such interpenetration of causal factors may be embodied by an array of organismal phenomena, including, as we shall discuss, culture’s relationships with the brain and the immune system. We propose reinterpreting immune function in this light, in particular the coupling of the individual immune system with larger, embedding structures.
The current vision of human biology among evolutionary anthropologists is consistent with Lewontin’s analysis and is summarized by Durham [11] as follows: 5 “...[G]enes and culture constitute two distinct but interacting systems of inheritance within human populations... [and] information of both kinds has influence, actual or potential, over ... behaviors [which] creates a real and unambiguous symmetry between genes and phenotypes on the one hand, and culture and phenotypes on the other... [G]enes and culture are best represented as two parallel lines or ‘tracks’ of hereditary influence on phenotypes...”
With regard to such melding, over hominid evolution genes came to encode for increasing hypersociality, learning, and language skills, so the complex cultural structures which better aid in buffering the local environment became widespread in successful populations [12]. Every successful human population seems to have a core of tool usage, sophisticated language, oral tradition, mythology and music, focused on relatively small family/extended family groupings of various forms. More complex social structures are build on the periphery of this basic genetic/cultural object [13]. At the level of the individual human, the genetic-cultural object appears to be mediated by what evolutionary psychologists postulate are cognitive modules within the human mind [14]. Each module was shaped by natural selection in response to specific environmental and social conundrums Pleistocene hunter-gatherers faced. One set of such domain-specific cognitive adaptations addresses problems of social interchange [15]. The human species’ very identity may rest, in part, on its unique evolved capacities for social mediation and cultural transmission. Anthropologist Robert Boyd has remarked that culture is as much a part of human biology as the enamel on our teeth. Indeed, a brain-and-culture condensation has been adopted as a kind of new orthodoxy in recent studies of human cognition. For example Nisbett et al. [16] review an extensive literature on empirical studies of basic cognitive differences between individuals raised in what they call ‘East Asian’ and ‘Western’ cultural heritages. They view Western-based pattern cognition as ‘analytic’ and East-Asian as ‘holistic.’ Nisbett et al. [16] find that 1. Social organization directs attention to some aspects of the perceptual field at the expense of others. 2. What is attended to influences metaphysics. 6 3. Metaphysics guides tacit epistemology, that is, beliefs about the nature of the world and causality. 4. Epistemology dictates the development and application of some cognitive processes at the expense of others. 5. Social organization can directly affect the plausibility of metaphysical assumptions, such as whether causality should be regarded as residing in the field vs. in the object. 6. Social organization and social practices can directly influence the development and use of cognitive processes such as dialectical vs. logical ones. Nisbett et al. [16] conclude that tools of thought embody a culture’s intellectual history, that tools have theories build into them, and that users accept these theories, albeit unknowingly, when they use these tools. We may assume, then, the existence of gene-culture and brain-culture condensations.
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