Homeostatic mechanisms

The number of known cytokines, as well as the diversity of biological functions, have led to a very complex and often confusing picture of the immunologic and nonimmunologic processes involved. The role of cytokiaes in local or systemic homeostatic mechanisms related to physiological functions may be utilized therapeutically for treatment of cancer and a variety of other diseases (2). Pharmaceutical research and development efforts surrounding lL-1 are typical examples of the cytokine inhibition approach to chronic inflammation research (2). 

HORMONES TRANSDUCE SIGNALS TO AFFECT HOMEOSTATIC MECHANISMS... 

Chopra I. (1988) EffliK of antibacterial agents finm bacteria. FEMS Symposium No. 44 Homeostatic Mechanisms of Microorganisms, pp. 146-58. Bahi Bahi University Press. 

Recent evidence indicates that the 5-HT transporter is subject to post-translational regulatory changes in much the same way as neurotransmitter receptors (Blakeley et al. 1998). Protein kinase A and protein kinase C (PKC), at least, are known to be involved in this process. Phosphorylation of the transporter by PKC reduces the Fmax for 5-HT uptake and leads to sequestration of the transporter into the cell, suggesting that this enzyme has a key role in its intracellular trafficking. Since this phosphorylation is reduced when substrates that are themselves transported across the membrane bind to the transporter (e.g. 5-HT and fi -amphetamine), it seems that the transport of 5-HT is itself linked with the phosphorylation process. Possibly, this process serves as a homeostatic mechanism which ensures that the supply of functional transporters matches the demand for transmitter uptake. By contrast, ligands that are not transported (e.g. cocaine and the selective serotonin reuptake inhibitors (SSRIs)) prevent the inhibition of phosphorylation by transported ligands. Thus, such inhibitors would reduce 5-HT uptake both by their direct inhibition of the transporter and by disinhibition of its phosphorylation (Ramamoorthy and Blakely 1999). 

Electrolytes are involved in many metabolic and homeostatic functions, including enzymatic and biochemical reactions, maintenance of cell membrane structure and function, neurotransmission, hormone function, muscle contraction, cardiovascular function, bone composition, and fluid homeostasis. The causes of electrolyte abnormalities in patients receiving PN may be multifactorial, including altered absorption and distribution excessive or inadequate intake altered hormonal, neurologic, and homeostatic mechanisms altered excretion via gastrointestinal and renal losses changes in fluid status and fluid shifts and medications. 

Sodium is the major extracellular cation. Because of its osmotic effects, changes in sodium content in the body have an important influence on extracellular fluid volume, including plasma volume. For example, excess sodium leads to the retention of water and an increase in plasma volume. Increased plasma volume then causes an increase in blood pressure. Conversely, sodium deficit leads to water loss and decreased plasma volume. A decrease in plasma volume then causes a decrease in blood pressure. Therefore, homeostatic mechanisms involved in the regulation of plasma volume and blood pressure involve regulation of sodium content, or sodium balance, in the body. 

There is ample support for the hypothesis of noradrenergic system dysfunction in depression however, the inconsistencies in findings rule out any simple model of increased or decreased noradrenergic activity. It is important to determine which noradrenergic system abnormalities relate specifically to the pathogenesis of mood disorders, and which are related to nonspecific effects of stress, homeostatic mechanisms, or comorbid psychopathology. More work is needed on the mood-state-depen-dence of noradrenergic function. 

Postural hypotension contributes to the risk of syncope and falls especially in the elderly (Verhaeverbeke and Mets 1997). In case of postural hypotension, drug treatment should always be reviewed. Due to a decrease in homeostatic mechanisms elderly more often have postural hypotension from drugs that lower blood pressure than younger patients (Turnheim 1998). It is not only cardiovascular drugs that may... 

While unicellular fungi do not require metal transport systems, multi-cellular fungi and plants most certainly do, and we consider their transport in plants, and then consider how metal ions are sequestered in storage compartments before addressing their homeostasis. Once again, we consider in turn these processes for iron, copper and zinc. Since iron metabolism has been most intensively studied in S. cerevisiae, of all the fungi, we will focus our attention on iron homeostatic mechanisms, however, as the reader will see shortly, copper and zinc homeostasis have many similarities. 

Both formalisms are only valid in the vicinity of a reference state and have inherent limits when dealing with small or vanishing concentrations. It is sometimes argued that this is no serious problem because homeostatic mechanisms keep the intracellular concentration in a limited range [318], However, this reasoning is not entirely convincing, because kinetic models are also and should be utilized to test and elucidate those mechanism, rather than presupposing them. 

The physiology of the autonomic nervous system. Most viscera are innervated by both divisions of the autonomic nervous system. In a sense they are antagonistic and as such are concerned with important homeostatic mechanisms. 

Homeostatic mechanisms also allow animals to control their intracellular pH very strictly. In humans for example, blood pH (usually taken as a reliable but indirect measure of cellular pH) is 7.4 0.04. At 37 °C cytosolic pH is actually slightly lower at about 7.0 but different compartments within the eukaryotic cells may have quite different pH, for example, lysosomes have an internal pH of about 5 the inside of a mitochondrion is more alkaline than the outside whilst the inside of a phagosome in a white blood cell is more acidic than its surrounding cytosol, both situations arising due to proton pumping across a membrane. 

Our questions broadened to consider how the transport and metabolic capabilities of these aquatic species compare with those of mammalian species. One reason for asking such a question is to assess whether the presence or absence of these capabilities alters the ability of fish to survive in toxic environments. Survival mechanisms fall into two catagories - behavioral and physiologic. An example of a behavioral mechanism could be as simple as a fish avoiding that area of a stream which contains toxic quantitites of phenol. When external perturbations caused by pollutants are small, homeostatic mechanisms such as those of the liver and kidney, allow fish to adapt to the body of water in which they exist. The problem then is related to defining the limits to which homeostatic phenomena can be stressed in aquatic species. An important reason to establish such information in fish is that bodies of water are the "ultimate sink" for a number of pollutants (12). Thus, while a behavioral response such as removing itself from a toxic environment is invariably available to a mammalian species, this type of response is impossible for a fish if a toxic xenobiotic occurs uniformly throughout an entire body of water. 

L.B. Willett and C.P. Hodgson of Ohio State University, in collaboration with the U.S. Department of Agriculture, are currently investigating reproductive, metabolic, and nutritional disorders following heptachlor exposure from contaminated food in cattle (FEDRIP 1990). These investigators will also determine the cellular alterations that can influence reproductive or other homeostatic mechanisms. 

Cell death pathways may be counteracted by survival signaling cascades in the early stages of intoxication or in cells that are resistant to the toxic actions of the drugs. Signaling via the transcription factor NF-kB may constitute such a homeostatic mechanism in the cochlea. Cells that survived aminoglycoside treatment in a model of chronic ototoxicity were marked by NF-kB activation. ... 

The most extreme manifestation of untreated hypothyroidism is myxedema coma, which even if detected early and appropriately treated, carries a mortality rate of 30 to 60%. Myxedema coma is a misnomer. Most patients exhibit neither the myxedema nor coma. Patients with myxedema coma usually have longstanding hypothyroidism with the classic symptoms of hypothyroidism. Decompensation into myxedema coma may occur when the homeostatic mechanisms of the severely hypothyroid patient are subject to a stressful precipitating event (e.g., infection, trauma, some medications, stroke, surgery). The principal manifestation of myxedema coma is a deterioration of mental status (apathy, confusion, psychosis, but rarely coma). Other common clinical features include hypothermia, diastolic hypertension (early), hypotension (late), hypoventilation, hypoglycemia, and hyponatremia. If myxedema coma is suspected, the patient is usually admitted to an intensive care unit for pulmonary and cardiovascular support... 

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