网范文：“A cognitive paradigm for gene expression” 关于诵读困难,最近探讨精神分裂症和自闭症,广泛支持的是大脑连通性模型，对这些疾病有相当大的兴趣，英语论文网站，从整体的角度来看，这篇医学范文认为，大脑连接操作的意识是至关重要的,在复杂的扩散张量磁共振成像的基础上探讨,认为精神分裂症是一种大规模的神经认知网络的障碍，而不是特定区域的病理变化，应该寻求结构和功能异常的描述，可能构成基础广泛的认知功能受损的疾病。
阅读障碍,改变阅读系统，和特定的大脑区域。这支持了这样一种观点，阅读障碍与大脑灰质有关。探讨假设镜像神经元系统,可能是负责共同注意力障碍,其次为语言延迟自闭症。下面的范文进行详述。
Recent research on schizophrenia, dyslexia, and autism, broadly supports a ‘brain connectivity’ model for these disorders that is of considerable interest from the perspective of global workspace/global broadcast models of consciousness that are the foundation of our work (e.g., Baars, 1989; Wallace, 2017), since large-scale brain connectivity is essential for the operation of consciousness, a principal, and very old, evolutionary adaptation (e.g., Wallace and Wallace, 2017). For example, Burns et al. (2017), on the basis of sophisticated diffusion tensor magnetic resonance imaging studies, argue that schizophrenia is a disorder of large-scale neurocognitive networks rather than specific regions, and that pathological changes in the disorder should be sought at the supra-regional level. Both structural and functional abnormalities in frontoparietal networks have been described and may constitute a basis for the wide range of cognitive functions impaired in the disorder, such as selective attention, language processing and attribution of agency. 7
Silani et al. (2017) find that, for dyslexia, altered activation observed within the reading system is associated with altered density of grey and white matter of specific brain regions, such as the left middle and inferior temporal gyri and left arcuate fasciculus. This supports the view that dyslexia is associated with both local grey matter dysfunction and with altered larger scale connectivity among phonological/reading areas. Villalobos et al. (2017) explore the hypothesis that large-scale abnormalities of the dorsal stream and possibly the mirror neuron system, may be responsible for impairments of joint attention, imitation, and secondarily for language delays in autism. Their empirical study showed that those with autism had significantly reduced connectivity with bilateral inferior frontal area 44, which is compatible with the hypothesis of mirror neuron defects in autism.
More generally, their results suggest that dorsal stream connectivity in autism may not be fully functional. Courchesne and Pierce (2017) suggest that, for autism, connectivity within the frontal lobe is excessive, disorganized, and inadequately selective, whereas connectivity between frontal cortex and other systems is poorly synchronized, weakly responsive and information impoverished. Increased local but reduced long-distance cortical-cortical reciprocal activity and coupling would impair the fundamental frontal function of integrating information from widespread and diverse systems and providing complex context-rich feedback, guidance and control to lower-level systems. Coplan (2017) has observed a striking pattern of excessive frontal lobe selfconnectivity in certain cases of anxiety disorder, and Coplan et al. (2017) find that maternal stress can affect long-term hippocampal neurodevelopment in a primate model.
As stated, brain connectivity is the sine qua non of Global Workspace/Broadcast models of individual mental function including consciousness (e.g., Baars, 1989; Wallace, 2017), and further analysis suggests that these disorders cannot be fully understood in the absence of a functional theory of consciousness, and in particular, of a detailed understanding of the elaborate regulatory mechanisms which must have evolved over the past half billion years to ensure the stability of that most central and most powerful of adaptations. For humans, of course, one of the principal regulatory mechanisms for mental function is the embedding culture and culturally-mediated social interaction, in addition to culture’s role as the second system of human heritage.
As the evolutionary anthropologist Robert Boyd has put it, culture is as much a part of human biology as the enamel on our teeth (e.g., Richerson and Boyd, 2017). Distortion of consciousness is not simply an epiphenomenon of the emotional dysregulation which many see as the ‘real’ cause of mental disorder.
Like the pervasive effects of culture, distortion of consciousness lies at the heart of both the individual experience of mental disorder and the effect of it on the embedding of the individual within both social relationships and cultural or environmental milieu. Yet the experience of individual consciousness cannot be disentangled from social interaction and culture (Wallace, 2017). Distortion of a culturally-mediated consciousness in mental disorders inhibits both rou- tine social interchange and the ability to meet internalized or expected cultural norms, a potentially destabilizing positive feedback.
Distortion of consciousness profoundly affects the ability to learn new, or change old, skills in the face of changing patterns of threat or opportunity, perhaps the most critical purpose of the adaptation itself. Distortion of consciousness causing decoupling from social and cultural context is usually a threat to long-term individual survival, and those with mental disorders significantly affecting consciousness typically experience severely shortened lifespans. Here we will expand recent explorations of a cognitive paradigm for gene expression (Wallace and Wallace, 2017, 2017) that incorporates the effects of surrounding epigenetic regulatory machinery as a kind of catalyst to include the effects of the embedding information source of human culture on the ontology of the human mind.
The essential feature is that a cognitive process, including gene expression, can instantiate a dual information source that can interact with the generalized language of culture in which, for example, social interplay and the interpretation of socioeconomic and environmental stressors, involve complicated matters of symbolism and its grammar and syntax. These information sources interact by a crosstalk that, over the life course, determines the ontology of mind, including its manifold dysfunctions. That is, contemporary American work on gene-environment interactions in psychiatry must be extended to the study of gene-culture-environment interactions. This is no small matter, and the probability models we present here are at the borders of current applied mathematics.
A cognitive paradigm for gene expression has emerged in which contextual factors determine the behavior of what Cohen characterizes as a ‘reactive system’, not at all a deterministic, or even stochastic, mechanical process (e.g., Cohen, 2017; Cohen and Harel, 2017; Wallace and Wallace, 2017, 2017). The very different formal approaches are, however, all in the spirit of Maturana and Varela (1980, 1992) who understood the central role that cognitive process must play across a vast array of biological phenomena. O’Nuallain (2017) has placed gene expression firmly in the realm of complex linguistic behavior, for which context imposes meaning, claiming that the analogy between gene expression and language production is useful both as a fruitful research paradigm and also, given the relative lack of success of natural language processing (nlp) by computer, as a cautionary tale for molecular biology.
A relatively simple model of cognitive process as an information source permits use of Dretske’s (1994) insight that any cognitive phenomenon must be constrained by the limit theorems of information theory, in the same sense that sums of stochastic variables are constrained by the Central Limit Theorem. This perspective permits a new formal approach to gene expression and its dysfunctions, in particular suggesting new and powerful statistical tools for data analysis that could contribute to exploring both ontology and its pathologies. Wallace and Wallace (2017, 2017) apply the perspective, respectively, to infec- tious and chronic disease. Here we extend the mathematical foundations of that work to examine the topological structures of development and developmental disorder, in the context of an embedding information source representing the compelling varieties of human culture.
This approach is consistent with the broad context of epigenetics and epigenetic epidemiology. In particular, Jablonka and Lamb (1995, 1998) argue that information can be transmitted from one generation to the next in ways other than through the base sequence of DNA. It can be transmitted through cultural and behavioral means in higher animals, and by epigenetic means in cell lineages. All of these transmission systems allow the inheritance of environmentally induced variation. Such Epigenetic Inheritance Systems are the memory systems that enable somatic cells of different phenotypes but identical genotypes to transmit their phenotypes to their descendants, even when the stimuli that originally induced these phenotypes are no longer present.
After a decade of research and debate, the epigenetic perspective has received much empirical confirmation (e.g., Backdahl et al. 2017; Turner, 2017; Jaenish and Bird, 2017; Jablonka, 2017). Foley et al. (2017) argue that epimutation is estimated to be 100 times more frequent than genetic mutation and may occur randomly or in response to the environment. Periods of rapid cell division and epigenetic remodeling are likely to be most sensitive to stochastic or environmentally mediated epimutation. Disruption of epigenetic profile is a feature of most cancers and is speculated to play a role in the etiology of other complex diseases including asthma allergy, obesity, type 2 diabetes, coronary heart disease, autism spectrum disorders and bipolar disorders and schizophrenia. Important work by Scherrer and Jost (2017a, b) that is similar to the approach of this explicitly invokes information theory in their extension of the definition of the gene to include the local epigenetic machinery, a construct they term the ‘genon’.
Their central point is that coding information is not simply contained in the coded sequence, but is, in their terms, provided by the genon that accompanies it on the expression pathway and controls in which peptide it will end up. In their view the information that counts is not about the identity of a nucleotide or an amino acid derived from it, but about the relative frequency of the transcription and generation of a particular type of coding sequence that then contributes to the determination of the types and numbers of functional products derived from the DNA coding region under consideration. The proper formal tools for understanding phenomena that ‘provide’ information – that are information sources – are the Rate Distortion Theorem and its zero error limit, the Shannon-McMillan Theorem.()
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