1+3 Covariant Cosmic Microwave Background anisotropies II: The almost - Friedmann Lemaitre model

This is the second of a series of papers extending the 1+3 covariant and gauge invariant treatment of kinetic theory to an examination of Cosmic Microwave Background temperature anisotropies arising from inhomogeneities in the early universe. The first paper dealt with algebraic issues. Here we derive the mode form of the integrated Boltzmann equations, first, giving a covariant version of the standard derivation using the mode recursion relations, second, demonstrating the link to the multipole divergence equations and finally various analytic ways of solving the resulting equations are discussed. A general integral form of solution is obtained for the equations with Thomson scattering. The covariant Friedmann-Lemaitre multipole form of the transport equations are found using the covariant and gauge-invariant generalization of the Peebles and Yu expansion in Thompson scattering time. The dispersion relations and damping scale are then obtained from the covariant approach. The equations are integrated to give the covariant and gauge-invariant equivalent of the canonical scalar sourced anisotropies. We carry out a simple treatment of the matter dominated free-streaming projection, slow decoupling, and tight-coupling cases, with the aim both giving a unified transparent derivation of this range of results and clarifying the connection between the more usual approaches (for example that of Hu and Sugiyama) and the treatment for scalar perturbations (for example the treatment of Challinor and Lasenby).Comment: To appear in Annals of Physic

Theories of schizophrenia: a genetic-inflammatory-vascular synthesis

BACKGROUND: Schizophrenia, a relatively common psychiatric syndrome, affects virtually all brain functions yet has eluded explanation for more than 100 years. Whether by developmental and/or degenerative processes, abnormalities of neurons and their synaptic connections have been the recent focus of attention. However, our inability to fathom the pathophysiology of schizophrenia forces us to challenge our theoretical models and beliefs. A search for a more satisfying model to explain aspects of schizophrenia uncovers clues pointing to genetically mediated CNS microvascular inflammatory disease. DISCUSSION: A vascular component to a theory of schizophrenia posits that the physiologic abnormalities leading to illness involve disruption of the exquisitely precise regulation of the delivery of energy and oxygen required for normal brain function. The theory further proposes that abnormalities of CNS metabolism arise because genetically modulated inflammatory reactions damage the microvascular system of the brain in reaction to environmental agents, including infections, hypoxia, and physical trauma. Damage may accumulate with repeated exposure to triggering agents resulting in exacerbation and deterioration, or healing with their removal. There are clear examples of genetic polymorphisms in inflammatory regulators leading to exaggerated inflammatory responses. There is also ample evidence that inflammatory vascular disease of the brain can lead to psychosis, often waxing and waning, and exhibiting a fluctuating course, as seen in schizophrenia. Disturbances of CNS blood flow have repeatedly been observed in people with schizophrenia using old and new technologies. To account for the myriad of behavioral and other curious findings in schizophrenia such as minor physical anomalies, or reported decreased rates of rheumatoid arthritis and highly visible nail fold capillaries, we would have to evoke a process that is systemic such as the vascular and immune/inflammatory systems. SUMMARY: A vascular-inflammatory theory of schizophrenia brings together environmental and genetic factors in a way that can explain the diversity of symptoms and outcomes observed. If these ideas are confirmed, they would lead in new directions for treatments or preventions by avoiding inducers of inflammation or by way of inflammatory modulating agents, thus preventing exaggerated inflammation and consequent triggering of a psychotic episode in genetically predisposed persons

Environmental exposure assessment of engineered nanoparticles : why REACH needs adjustment

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