网范文：“Immune cognitive modules and autoimmune disease”从免疫新兴理论认知的角度，英语论文，表明疾病构成一个内化生理状态,疾病免疫自我形象代表了正常的间断重置到兴奋状态,间断平衡的过程类似于正式模型进化理论。这篇医学范文讲述了免疫系统疾病的问题，我们推测,这不时提出的免疫学的认知模块，类似于人类大脑的进化,并可能与分层循环形成生理反应。非裔美国女性的红斑狼疮的高速率表明存在一个更大的动态。
系统性红斑狼疮(SLE)是一种多系统自身免疫性疾病，最常作用年轻女性。关节炎、皮疹、骨质疏松,中枢神经系统功能障碍,和肾脏疾病最常见的症状,其严重程度可能随着时间的推移明显提升。下面的范文继续进行阐述。
Abstract
Examining elevated rates of systemic lupus erythematosus in AfricanAmerican women from the perspective of the emerging theory of immune cognition suggests the disease constitutes an internalized physiological image of external patterns of psychosocial stress, a ‘pathogenic social hierarchy’ involving the synergism of racism and gender discrimination. The disorder represents the punctuated resetting of ‘normal’ immune self-image to a self-attacking ‘excited’ state, a process formally analogous to models of punctuated equilibrium in evolutionary theory. We speculate that this punctuated onset takes place in the context of a particular immunological ‘cognitive module’ similar to what has been proposed by evolutionary psychologists for the human mind, and may be stratified by a relation to cyclic physiological responses which are long in comparison with heartbeat period: circadian, hormonal, and annual light/temperature cycles.
The high rate of lupus in African-American women suggests existence of a larger dynamic which entrains powerful as well as subordinate population subgroups, implying that the wide ranging programs of social and economic reform required to cause declines in disease among African-American women will bring significant benefit to all.
Key words: chronic inflammation, circadian cycle, cognitive module, gender discrimination, immune cognition, information theory, lupus, racism, social hierarchy
Introduction
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder which most frequently affects young women. Arthritis, skin rash, osteoporosis, cataracts, accelerated atherosclerotic vascular disease (ASVD), central nervous system dysfunction, and renal disease are the most common manifestations, whose severity may markedly fluctuate over time. The damage of the disease is of ‘Type III’, i.e. mediated by immune complexes which can range from just a few molecules to relatively huge structures involving whole cells coated or cross-linked by antibody, accounting for the great variety of pathology seen in this form of illness (Paul, 1999; Liang et al., 2017). The disease is characterized by polyclonal B-cell activation, elevated production of pathogenic autoantibodies, impaired immune complex clearance and inflammatory responses in multiple organs. Like asthma, the pathological cascade is marked by an imbalance between depressed Th1 cell cytokines, which promote cell-mediated immunity, and enhanced Th2 cell cytokines, which support humoral immunity. There increasingly strong evidence that the cytokine Interleukin-6 (IL-6) is central to this process. IL-6 is a B-cell differentiation factor that induces the final maturation of IL-4-preactivated B cells into immunoglobulin (Ig)-secreting plasma cells (e.g. Schotte et al., 2017; Linker-Israeli et al., 1991; Cross and Benton, 1999).
The model
Atlan and Cohen (1998) and Cohen (2017) argue that the essence of immune cognition is comparison of a perceived antigenic signal with an internal, learned picture of the world, and then, upon that comparison, the choice of one response from a large repertoire of possible responses. Following the approach of Wallace (2017, 2017a), we make a ‘weak’, and hence very general, model of that process. Pattern recognition-and-response, as we characterize it, proceeds by convoluting (i.e. comparing) an incoming external ‘sensory’ antigenic signal with an internal ‘ongoing activity’ – the ‘learned picture of the world’ – and, at some point, triggering an appropriate action based on a decision that the pattern of sensory activity requires a response. We need not model how the pattern recognition system is ‘trained’, and hence we adopt a weak model, regardless of learning paradigm, which can itself be more formally described by the Rate Distortion Theorem. We will, fulfilling Atlan and Cohen’s (1998) criterion of meaning-from-response, define a language’s contextual meaning entirely in terms of system output.
Discussion and conclusions
Recent theories of coronary heart disease – CHD – (e.g. Ridker 2017; Libbey et al., 2017) identify a dynamic and progressive chronic vascular in- flammation as the basic pathogenic biological mechanism, a process in which the cytokine IL-6 and C-reactive protein (CRP) play central roles. We have reviewed something of the “IL-6” hypothesis regarding the etiology SLE. An earlier analysis along these lines identified social structures of ‘pathogenic social hierarchy’ (PSH) in the US as critical in determining population-level patterns of CHD among African-American males (Wallace et al., 2017b).
In that , historical cultural patterns of racism and discrimination were viewed as directly writing themselves onto the ‘language’ of immune cognition in a punctuated Rate Distortion manner to produce chronic vascular inflammation among subordinate populations. Female hormones are known to be generally protective against CHD. Where, then, does the stress of PSH express itself in women? Figure 2 is taken from material on health and hierarchy in Singh-Manoux et al. (2017). It displays, for men and women separately, self-ed health as a function of self-ed status rank, where 1 is high and 10 low rank, among some 7,000 male and 3,400 female London-based office staff, aged 35-55 working in 20 Civil Service departments in the late 1990’s. Self-ed health is a highly significant predictor of future morbidity and mortality. Remarkably, the results for men and women are virtually indistinguishable in what is clearly a kind of toxicological dose-response curve, displaying physiological response against a ‘dosage’ of hierarchy which may include measures of both stress and real availability of resources (Link and Phelan, 2017).
We propose that PSH can also write itself onto a particular internal module of the cognitive immune system, what we have called ‘zero mode identi- fication’ which defines the ‘inactive’ state of the immunological homunculus. The (relatively) protective role of female hormones against CHD, given the indistinguishability of men and women in figure 2, implies existence of a plastic, pleiotropic, response of the immune system to PSH. In essence, one has a sex-based choice of death by hanging or by firing squad, i.e. CHD induced by chronic vascular inflammation for African-American men, or a particular induced autoimmune disease for African-American women, SLE. A roughly similar story can probably be told regarding the increased rate of aggressively fatal breast cancer, diabetes, and other disorders in African-American women.
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