The CEMI Field Theory Closing the Loop

Several theories of consciousness first described about a decade ago, including the conscious electromagnetic information (CEMI) field theory, claimed that the substrate of consciousness is the brain's electromagnetic (EM) field. These theories were prompted by the observation, in many diverse systems, that synchronous neuronal firing, which generates coherent EM fields, was a strong correlate of attention, awareness, and consciousness. However, when these theories were first described there was no direct evidence that synchronous firing was actually functional, rather than an epiphenomenon of brain function. Additionally, any EM field-based consciousness would be a 'ghost in the machine' unless the brain's endogenous EM field is also able to influence neuron firing. Once again, when these theories were first described, there was only indirect evidence that the brain's EM field influenced neuron firing patterns in the brain. In this paper I describe recent experimental evidence which demonstrate that synchronous neuronal firing does indeed have a functional role in the brain; and also that the brain's endogenous EM field is involved in recruiting neurons to synchronously firing networks. The new data point to a new and unappreciated form of neural communication in the brain that is likely to have significance for all theories of consciousness. I describe an extension of the CEMI field theory that incorporates these recent experimental findings and integrates the theory with the 'communication through coherence' hypothesis

Consciousness: Matter or EMF?

Conventional theories of consciousness (ToCs) that assume that the substrate of consciousness is the brain's neuronal matter fail to account for fundamental features of consciousness, such as the binding problem. Field ToC's propose that the substrate of consciousness is the brain's best accounted by some kind of field in the brain. Electromagnetic (EM) ToCs propose that the conscious field is the brain's well-known EM field. EM-ToCs were first proposed only around 20 years ago primarily to account for the experimental discovery that synchronous neuronal firing was the strongest neural correlate of consciousness (NCC). Although EM-ToCs are gaining increasing support, they remain controversial and are often ignored by neurobiologists and philosophers and passed over in most published reviews of consciousness. In this review I examine EM-ToCs against established criteria for distinguishing between ToCs and demonstrate that they outperform all conventional ToCs and provide novel insights into the nature of consciousness as well as a feasible route toward building artificial consciousnesses

The CEMI Field Theory Gestalt Information and the Meaning of Meaning

In earlier papers I described the conscious electromagnetic information (CEMI) field theory, which claimed that the substrate of consciousness is the brain's electromagnetic (EM) field. I here further explore this theory by examining the properties and dynamics of the information underlying meaning in consciousness. I argue that meaning suffers from a binding problem, analogous to the binding problem described for visual perception, and describe how the gestalt (holistic) properties of meaning give rise to this binding problem. To clarify the role of information in conscious meaning, I differentiate between extrinsic information that is symbolic and arbitrary, and intrinsic information, which preserves structural aspects of the represented object and thereby maintains some gestalt properties of the represented object. I contrast the requirement for a decoding process to extract meaning from extrinsic information, whereas meaning is intrinsic to the structure of the gestalt intrinsic information and does not require decoding. I thereby argue that to avoid the necessity of a decoding homunculus, conscious meaning must be encoded intrinsically -- as gestalt information -- in the brain. Moreover, I identify fields as the only plausible substrate for encoding gestalt intrinsic information and argue that the binding problem of meaning can only be solved by grounding meaning in this field-based gestalt information. I examine possible substrates for gestalt information in the brain and conclude that the only plausible substrate is the CEMI field

Slow protein fluctuations explain the emergence of growth phenotypes and persistence in clonal bacterial populations

One of the most challenging problems in microbiology is to understand how a small fraction of microbes that resists killing by antibiotics can emerge in a population of genetically identical cells, the phenomenon known as persistence or drug tolerance. Its characteristic signature is the biphasic kill curve, whereby microbes exposed to a bactericidal agent are initially killed very rapidly but then much more slowly. Here we relate this problem to the more general problem of understanding the emergence of distinct growth phenotypes in clonal populations. We address the problem mathematically by adopting the framework of the phenomenon of so-called weak ergodicity breaking, well known in dynamical physical systems, which we extend to the biological context. We show analytically and by direct stochastic simulations that distinct growth phenotypes can emerge as a consequence of slow-down of stochastic fluctuations in the expression of a gene controlling growth rate. In the regime of fast gene transcription, the system is ergodic, the growth rate distribution is unimodal, and accounts for one phenotype only. In contrast, at slow transcription and fast translation, weakly non-ergodic components emerge, the population distribution of growth rates becomes bimodal, and two distinct growth phenotypes are identified. When coupled to the well-established growth rate dependence of antibiotic killing, this model describes the observed fast and slow killing phases, and reproduces much of the phenomenology of bacterial persistence. The model has major implications for efforts to develop control strategies for persistent infections.Comment: 26 pages, 7 figure

Towards the Immunoproteome of Neisseria meningitidis

Despite the introduction of conjugated polysaccharide vaccines for many of the Neisseria meningitidis serogroups, neisserial infections continue to cause septicaemia and meningitis across the world. This is in part due to the difficulties in developing a, cross-protective vaccine that is effective against all serogroups, including serogroup B meningococci. Although convalescent N. meningitidis patients develop a natural long-lasting cross-protective immunity, the antigens that mediate this response remain unknown. To help define the target of this protective immunity we identified the proteins recognized by IgG in sera from meningococcal patients by a combination of 2D protein gels, western blots and mass spectrometry. Although a number of outer membrane antigens were identified the majority of the antigens were cytoplasmic, with roles in cellular processes and metabolism. When recombinant proteins were expressed and used to raise sera in mice, none of the antigens elicited a positive SBA result, however flow cytometry did demonstrate that some, including the ribosomal protein, RplY were localised to the neisserial cell surface

Design of double-walled carbon nanotubes for biomedical applications

Double-walled carbon nanotubes (DWNTs) prepared by catalytic chemical vapour deposition were functionalized in such a way that they were optimally designed as a nano-vector for the delivery of small interfering RNA (siRNA), which is of great interest for biomedical research and drug development. DWNTs were initially oxidized and coated with a polypeptide (Poly(Lys:Phe)), which was then conjugated to thiol-modified siRNA using a heterobifunctional cross-linker. The obtained oxDWNT–siRNA was characterized by Raman spectroscopy inside and outside a biological environment (mammalian cells). Uptake of the custom designed nanotubes was not associated with detectable biochemical perturbations in cultured cells, but transfection of cells with DWNTs loaded with siRNA targeting the green fluorescent protein (GFP) gene, serving as a model system, as well as with therapeutic siRNA targeting the survivin gene, led to a significant gene silencing effect, and in the latter case a resulting apoptotic effect in cancer cells

Interrogation of global mutagenesis data with a genome scale model of Neisseria meningitidis to assess gene fitness in vitro and in sera

BACKGROUND: Neisseria meningitidis is an important human commensal and pathogen that causes several thousand deaths each year, mostly in young children. How the pathogen replicates and causes disease in the host is largely unknown, particularly the role of metabolism in colonization and disease. Completed genome sequences are available for several strains but our understanding of how these data relate to phenotype remains limited. RESULTS: To investigate the metabolism of N. meningitidis we generated and selected a representative Tn5 library on rich medium, a minimal defined medium and in human serum to identify genes essential for growth under these conditions. To relate these data to a systems-wide understanding of the pathogen's biology we constructed a genome-scale metabolic network: Nmb_iTM560. This model was able to distinguish essential and non-essential genes as predicted by the global mutagenesis. These essentiality data, the library and the Nmb_iTM560 model are powerful and widely applicable resources for the study of meningococcal metabolism and physiology. We demonstrate the utility of these resources by predicting and demonstrating metabolic requirements on minimal medium such as a requirement for PEP carboxylase, and by describing the nutritional and biochemical status of N. meningitidis when grown in serum, including a requirement for both the synthesis and transport of amino acids. CONCLUSIONS: This study describes the application of a genome scale transposon library combined with an experimentally validated genome-scale metabolic network of N. meningitidis to identify essential genes and provide novel insight to the pathogen's metabolism both in vitro and during infection