Stress is a ubiquitous and pervasive part of modern life that is frequently blamed for causing a plethora of diseases and other discomforting medical conditions. All higher organisms, including humans, experience stress in the form of a wide variety of stressors that range from environmental pollutants and drugs to traumatic events or self-induced trauma. Stressors registered by the central nervous system (CNS) generate physiological stress responses in the body (periphery) by means of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis. This LHPA axis operates through the use of chemical messengers such as the stress hormones corticotropin-releasing hormone (CRH) and glucocorticoids (GCs). Under conditions of frequent exposure to acute stress and/or chronic, long-term exposure to stress, the LHPA axis becomes dysfunctional and in the process frequently overproduces both CRH and GCs, which results in many mild to severely toxic side effects. Bidirectional communication between the LHPA axis and immune/inflammatory systems can dramatically potentiate these side effects and create environments in the CNS and periphery ripe for the triggering and/or promotion of tissue degeneration and disease. This review aims to present as far as possible a molecular view of the processes involved so as to provide a bridge from the diffuse range of studies on molecular structure and receptor interactions to the burgeoning biological and medical literature that describes the empirical interplay between stress and disease. We hope that our review of this fast-growing field, which we christen chemical neuroimmunology, will give a clear indication of the striking range and depth of current molecular, cellular and medical evidence linking stress hormones to degeneration and disease. In so doing, we hope to provide encouragement for others to become interested in this critical and far-reaching field of research, which is very much at the heart of many important disease processes and very much a critical part of the crucial interface between chemistry and biology.
A model of the inlet section of hydrodynamic flow stabilization is proposed. The expanse of the zone of extremal flow restructuring is evaluated numerically for the section of hydrodynamic stabilization within the limits of which the height of the bundle of a regular packing should be assigned.Regular packings formed from individual crimped plates, which are assembled into bundles, have come into widespread use for heat-and mass-exchange processes in tower equipment employed by the chemical and other branches of industry. The channels that are formed here assume different shapes. At the present time, use of the so-called terminal effects, which are based on familiar laws governing restructuring of the velocity field of gaseous and liquid flows at the inlet to and outlet from channels of any shape during the development of effective regular packings is particularly urgent, since the assurance of high effectiveness of heat and mass exchange is rendered possible with a shallower layer of packing [1].A diaphragm model permitting evaluation of the length of the inlet section of hydrodynamic flow stabilization in a channel type of regular packing is proposed in this study.Numerical assessment of the length L hst of hydrodynamic flow stabilization assumes major significance for aerodynamic optimization of the shape and linear dimensions of the channels in regular structured packings. This section is even observed in vessels with a complex channel geometry, for example, in vessels with a stationary granular bed, and also in heat exchangers with a transverse flow past a tube bundle [2]. As applies to regular packings, evaluation of the length L hst is discussed in [2].In vessels designed for chemical production, the inlet section of hydrodynamic gaseous-flow stabilization is observed in channels of regular and irregular packings. The current of this flow within the space of intergrain passages of irregular packings is characterized by a higher degree of meandering and a variable section of the channels throughout their length as compared with the inclined channels of regular structured packings [5]. As is noted in [3,6], moreover, the length of the inlet section of hydrodynamic flow stabilization in the case of an irregular packing is clearly defined by the length of formation of the statistically stable geometric structure of the placement of the components in the irregular packing, i.e., the channel geometry.
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