Predicting Health Impacts of the World Trade Center Disaster: 1. Halogenated hydrocarbons, symptom syndromes, secondary victimization, and the burdens of history

The recent attack on the World Trade Center, in addition to direct injury and psychological trauma, has exposed a vast population to dioxins, dibenzofurans, related endocrine disruptors, and a multitude of other physiologically active chemicals arising from the decomposition of the massive quantities of halogenated hydrocarbons and other plastics within the affected buildings. The impacts of these chemical species have been compounded by exposure to asbestos, fiberglass, crushed glass, concrete, plastic, and other irritating dusts. To address the manifold complexities of this incident we combine recent theoretical perspectives on immune, CNS, and sociocultural cognition with empirical studies on survivors of past large toxic fires, other community-scale chemical exposure incidents, and the aftereffects of war. Our analysis suggests the appearance of complex, but distinct and characteristic, spectra of synergistically linked social, psychosocial, psychological and physical symptoms among the 100,000 or so persons most directly affected by the WTC attack. The different 'eigenpatterns' should become increasingly comorbid as a function of exposure. The expected outcome greatly transcends a simple 'Post Traumatic Stress Disorder' model, and may resemble a particularly acute form of Gulf War Syndrome. We explore the role of external social factors in subsequent exacerbation of the syndrome -- secondary victimization -- and study the path-dependent influence of individual and community-level historical patterns of stress. We suggest that workplace and other organizations can act as ameliorating intermediaries. Those without acess to such buffering structures appear to face a particularly bleak future

Selection pressure and organizational cognition: implications for the social determinants of health

We model the effects of Schumperterian 'selecton pressures' -- in particular Apartheid and the neoliberal 'market economy' -- on organizational cognition in minority communities, given the special role of culture in human biology. Our focus is on the dual-function social networks by which culture is imposed and maintained on individuals and by which immediate patterns of opportunity and threat are recognized and given response. A mathematical model based on recent advances in complexity theory displays a joint cross-scale linkage of social, individual central nervous system, and immune cognition with external selection pressure through mixed and synergistic punctuated 'learning plateaus.' This provides a natural mechanism for addressing the social determinants of health at the individual level. The implications of the model, particularly the predictions of synergistic punctuation, appear to be empirically testable

Immune cognition, social justice and asthma: structured stress and the developing immune system

We explore the implications of IR Cohen's work on immune cognition for understanding rising rates of asthma morbidity and mortality in the US. 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. 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

Life as an Explanation of the Measurement Problem

No consensus regarding the universal validity of any particular interpretation of the measurement problem has been reached so far. The problem manifests strongly in various Wigner's-friend-type experiments where different observers experience different realities measuring the same quantum system. But only classical information obeys the second law of thermodynamics and can be perceived solely at the holographic screen of the closed orientable two-dimensional manifold implied by Verlinde's and Landauer's mass-information equivalence equations. I conjecture that biological cell, as a dissipative structure, is the smallest agent capable of processing quantum information through its holographic screen and that this mechanism have been extended by natural evolution to endo- and exosemiosis in multicellular organisms, and further to language of Homo sapiens. Any external stimuli must be measured and classified by the cell in the context of classical information to provide it with an evolutionary gain. Quantum information contained in a pure quantum state cannot be classified, while incoherent mixtures of non-orthogonal quantum states are only partially classifiable. The concept of an unobservable velocity, normal to the holographic screen is introduced. It is shown that it enables to derive the Unruh acceleration as acting normal to the screen, as well as to conveniently relate de Broglie and Compton wavelengths. It follows that the perceived universe, is induced by the set of Pythagorean triples, while all its measurable features, including perceived dimensionality, are set to maximise informational diversity.Comment: This research is incomplete and partially incorrec

c-Jun N-Terminal Kinase in Inflammation and Rheumatic Diseases.

The c-Jun N-terminal kinases (JNKs) are members of the mitogen-activated protein kinase (MAPK) family and are activated by environmental stress. JNK is also activated by proinflammatory cytokines, such as TNF and IL-1, and Toll-like receptor ligands. This pathway, therefore, can act as a critical convergence point in immune system signaling for both adaptive and innate responses. Like other MAPKs, the JNKs are activated via the sequential activation of protein kinases that includes two dual-specificity MAP kinase kinases (MKK4 and MKK7) and multiple MAP kinase kinase kinases. MAPKs, including JNKs, can be deactivated by a specialized group of phosphatases, called MAP kinase phosphatases. JNK phosphorylates and regulates the activity of transcription factors other than c-Jun, including ATF2, Elk-1, p53 and c-Myc and non-transcription factors, such as members of the Bcl-2 family. The pathway plays a critical role in cell proliferation, apoptosis, angiogenesis and migration. In this review, an overview of the functions that are related to rheumatic diseases is presented. In addition, some diseases in which JNK participates will be highlighted

W. M. Keck Foundation 2010 Annual Report

Contains board chair's message, 2010 program highlights and grantee profiles, grants list, financial statements, and lists of board members and committee members

Noise in multiple sclerosis: unwanted and necessary

As our knowledge about the etiology of multiple sclerosis (MS) increases, deterministic paradigms appear insufficient to describe the pathogenesis of the disease, and the impression is that stochastic phenomena (i.e. random events not necessarily resulting in disease in all individuals) may contribute to the development of MS. However, sources and mechanisms of stochastic behavior have not been investigated and there is no proposed framework to incorporate nondeterministic processes into disease biology. In this report, we will first describe analogies between physics of nonlinear systems and cell biology, showing how small-scale random perturbations can impact on large-scale phenomena, including cell function. We will then review growing and solid evidence showing that stochastic gene expression (or gene expression “noise”) can be a driver of phenotypic variation. Moreover, we will describe new methods that open unprecedented opportunities for the study of such phenomena in patients and the impact of this information on our understanding of MS course and therapy

The neurobiological effects of ocean acidification on a cephalopod

Jodi Thomas investigated the response of the squid nervous system to elevated carbon dioxide (CO2). She found that a complex assortment of multiple mechanisms likely underpins behavioural and physiological responses to elevated CO2. This mechanistic understanding will help identify which animals will be most vulnerable to rising seawater CO2 levels