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PubMed2000

Developmental changes in metabotropic glutamate receptor-mediated calcium homeostasis.

Neurons of the chick cochlear nucleus, nucleus magnocellularis (NM), require eighth nerve activation of metabotropic glutamate receptors (mGluRs) for maintenance of intracellular calcium homeostasis. Interrupting this activation results in an increase in intracellular calcium concentration ([Ca(2+)](i)) followed by cell atrophy, degeneration, and death of many neurons. Although these phenomena are well characterized in late embryonic and posthatch chicks, little is known about the role of mGluRs and calcium homeostasis during the development of synaptic activity in NM. Using Fura-2 imaging, fluorescent immunohistochemistry, and Western immunoblotting, we investigated (1) the expression and function of group I mGluRs and their role in calcium regulation during development of NM, and (2) the expression of two other key molecules involved in regulating neuronal [Ca(2+)](i) : inositol trisphosphate receptors (IP(3)Rs) and sarcoplasmic/endoplasmic reticulum calcium ATPases (SERCAs). Confocal imaging of Fluo-3-labeled NM was used to investigate the kinetics of global NM neuron calcium signals. Measurements were made at four ages that extend from before synaptic function begins in NM, through functional onset, to mature patterns of spontaneous activity, namely, embryonic days (E) 10, 13, 15, and 18. mGluR5, mGluR1, and SERCA expression peaked at E13 and then decreased with age. IP(3)R expression increased to peak at E18. [Ca(2+)](i) response to mGluR activation increased with age. The rise time of [Ca(2+)](i) signals in NM neurons did not change with development, but E13 neurons were slower to reestablish baseline [Ca(2+)](i). These results suggest that the mGluR-mediated calcium homeostasis of NM neurons develops in parallel with synaptic activity and appears to be refined with increasing synaptic activity.

Aging↗

PubMed2000

Sleep homeostasis and the function of sleep.

A considerable number of hypothetical functions of sleep have been proposed, but none of the hypotheses under active consideration has gained enough experimental support to convince a preponderance of sleep researchers. Some researchers even question whether we should expect to identify one primary function of sleep, given the multitude of physiological processes that are affected by sleep. But we do know that sleep is homeostatically regulated, and we have discovered a great deal about the physiological mechanisms underlying sleep homeostasis. Other homeostatically regulated behaviors have one or a small number of functions, and those functions are closely linked to the homeostatic control mechanisms for those process. We can therefore apply what is already known about sleep homeostasis to test and evaluate hypothesized functions of sleep. It should be possible to trace the connections between the cellular and molecular basis of a hypothesized function and the cellular and molecular mechanisms underlying homeostatic responses to sleep deprivation. Hypothesized functions that do not plausibly admit of such connections can reasonably be rejected. Four current hypotheses suggesting that the function of sleep is to assist in the process of activity-dependent synaptic reorganization are critiqued to demonstrate how what is known about sleep homeostasis can be used to assess hypothesized functions of sleep.

Brain↗

PubMed2000

Mechanisms of destabilization of Ca2+-homeostasis of brain neurons caused by toxic glutamate challenge.

The long-term stimulation of mammalian central neurons with an excitatory neuromediator, glutamate, results in destabilization of Ca2+-homeostasis caused mainly by an impairment of the systems of excessive Ca2+ extrusion from the cytoplasm both into the environment (Na+/Ca2+-exchanger, Ca2+/H+ pump) and mitochondria. The data available suggest that inhibition of the mitochondrial Ca2+ uptake following the glutamate action is due to the strong depolarization of inner mitochondrial membrane caused by opening of the "large pore" in response to the Ca2+ overload and overproduction of free oxygen radicals and NO. The mechanism of deterioration of Ca2+ extrusion from the neuron into extracellular medium following the glutamate challenge has not been yet fully clarified. It is only known that some factors inhibiting or irreversibly altering the functions of Na+/Ca2+-exchanger and Ca2+/H+ pump are accumulated in the cell during the prolonged action of glutamate. They include lowering of ATP concentration and pHi, as well as overproduction of free oxygen radicals and products of lipid peroxidation. The exact contribution of these factors to the final destabilization of Ca2+ homeostasis is under study. A good correlation between the glutamate-induced mitochondrial depolarization and the failure of neurons to extrude excessive Ca2+ from the cytoplasm during the post-glutamate period indicates that at this period the mitochondrial dysfunction is critical for the destabilization of Ca2+ homeostasis.

Animals↗

PubMed2000

Iron homeostasis: new tales from the crypt.

The enterocyte is a highly specialized cell of the duodenal epithelium that coordinates iron uptake and transport into the body. Until recently, the molecular mechanisms underlying iron absorption and iron homeostasis have remained a mystery. This review focuses on the proteins and regulatory mechanisms known to be present in the enterocyte precursor cell and in the mature enterocyte. The recent cloning of a basolateral iron transporter and investigations into its regulation provide new insights into possible mechanisms for iron transport and homeostasis. The roles of proteins such as iron regulatory proteins, the hereditary hemochromatosis protein (HFE)-transferrin receptor complex, and hephaestin in regulating this transporter and in regulating iron transport across the intestinal epithelium are discussed. A speculative, but testable, model for the maintenance of iron homeostasis, which incorporates the changes in the iron-related proteins associated with the life cycle of the enterocyte as it journeys from the crypt to the tip of the villous is proposed.

Anemia, Hypochromic↗

PubMed2003

Immunoregulation by Vbeta specific antibodies in myasthenia gravis: mining physiological T cell homeostasis for TCR specific therapy.

Besides regulatory T cells, also comprising T cell receptor (CR)-specific T cells, it is increasingly evident that natural autoantibodies, among which anti-TCR antibodies represent additional immunomodulators in the immune system. We took advantage of myasthenia gravis (MG), a well-characterized antibody-mediated autoimmune disease, to demonstrate that without prior vaccination against TCR determinants, patients with MG present increased circulating anti-TCR antibodies directed to the dominant TCR used by pathogenic T cells. These findings, pointing to a regulatory protective role of anti-TCR antibodies, are discussed in the context of the mechanisms of action and the physiological role of anti-TCR antibodies in T cell homeostasis, and of the puzzling world of regulatory T cells. Natural anti-TCR antibodies are found in the serum of all individuals, with prevalence in physiological and pathological situations such as ageing, pregnancy, allograft transplantation, retroviral infection, and autoimmune diseases, including MG. The common link is the mounting of immune responses against alloantigens, pathogens or autoantigens, conferring on anti-TCR antibodies a broader role in controlling responses to any antigen (self or non-self) and more generally in T cell homeostasis. This homeostasis mechanism may well be exploited in therapeutic strategies based on TCR peptide vaccination in autoimmune diseases.

Animals↗

PubMedDate not supplied

[Features of antioxidative homeostasis in different lipid metabolic changes in patients with coronary vessel arteriosclerosis].

In patients with atherosclerosis of coronary vessels, particular features of antioxidative homeostasis which reflect dynamic balance between reactions of peroxide oxidation of lipids and those of the antioxidant system were studied. Different mechanisms have been revealed of maintenance of antioxidative homeostasis in patients with atherosclerosis of coronary vessels depending on the type of lipid abnormalities. In calculating the coefficient of significance (Kj) formulas have been deduced of significant parameters of antioxidative homeostasis in those atherosclerotic patients revealing normolipidemia, dyslypoproteidemia, type II and IV, that can be used as additional diagnostic and prognostic criteria for the course of the atherosclerotic process.

Adult↗

PubMed2004

[Molecular mechanism of epimedium flavonoids in immune homeostasis remodeling in aged rats revealed by lymphocyte gene expression profile].

OBJECTIVE: To elucidate the gene regulatory pattern of Epimedium flavonoids (EF) in immune homeostasis remodeling in the aged rats. METHODS: (1) To quantitatively analyse the apoptosis percentage of lymphocyte in spleen of aged, young and EF treated rats using flow cytometry. (2) To analyse the lymphocyte gene expression profiles of different groups using gene chips (Rat Genome U34A). RESULTS: (1) Detection of lymphocyte apoptosis percentage showed that there was significant difference in comparing between aged group and young group, between EF treated group and aged group (P < 0.01). (2) As compared with that in the young group, in the aged group, 116 genes were up-regulated and 215 down-regulated. As compared with that in the old group, in the EF treated group, 447 genes were up-regulated and 456 down-regulated, which involved the aspects as cell apoptosis and cell proliferation regulation, etc. CONCLUSION: (1) The expression pattern characterized by up-regulation of apoptosis promoting genes expression and down-regulation of apoptosis inhibiting genes expression, is the important gene background of immuno-homeostasis imbalance in the aged. (2) The role of EF is to reverse the abnormal changes of gene expressions with opposite functions, i.e. the apoptosis promoting and inhibiting, proliferation enhancing and antagonizing genes, to reconstruct a beneficial equilibrium of gene expression and thus to further remodel the immuno-homeostasis in the aged.

Adjuvants, Immunologic↗

PubMed2004

Alterations in calcium homeostasis as biological marker for mild Alzheimer's disease?

The calcium hypothesis of neurodegenerative disorders such as Alzheimer's disease (AD) suggests that altered cytosolic Ca(2+) levels ( Ca(2+) (i)) and/or disturbances in Ca2+ homeostasis concern cellular mechanisms underlying neuronal pathology. To search for a diagnostic marker of Alzheimer's disease, we measured cytosolic calcium concentrations in platelets of AD patients, age-matched control subjects (AMC), and vascular dementia (VD) patients. The ( Ca(2+) (i)) was determined using long wavelength indicator Fluo-3AM in 21 mild AD patients, 17 AMC, and 23 patients with VD. The basal values of [Ca(2+)](i) were significantly lower in AD compared to AMC. After the addition of 1 mM calcium, the [Ca(2+)](i) markedly increased in platelets of AD compared to AMC and VD. Measurement of calcium homeostasis could provide a very sensitive, but less specific biological marker of AD. These results support the hypothesis that influencing calcium homeostasis may provide a therapeutic strategy in dementia.

Aged↗

PubMedDate not supplied

[Some general pathological and biological categories: health, disease, homeostasis, sanogenesis, adaptation, immunity. New approaches and definitions].

The article outlines new approaches to definition of categories of homeostasis, health, disease and sanogenesis in terms of relationships between human body and environment. According to these definitions, health is the state of the body with unaffected functional dynamic homeostasis securing optimal functioning for productive relations with the environment; disease is the state of the body with affected functional dynamic homeostasis and its inability to accomplish functions for productive relations with the environment. These formulations reflect biological and social aspects of the above categories.

Adaptation, Physiological↗

PubMed2006

[The role of reactive oxygen and nitrogen species in calcium and iron homeostasis dysregulation in anthracycline cardiotoxicity].

Anthracyclines are potent anticancer agents which have been used in therapy for 40 years. However, their activity is very limited due to their cumulative, dose-dependent, chronic cardiotoxicity. The cardiotoxic effect of anthracyclines may lead to irreversible and incurable cardiomyopathy, which impairs quality of live and increases the risk of death. The most prominent feature of this cardiac disease is diminished ejection fraction of the left ventricle, which leads to congestive heart failure. Reactive oxygen species, alcoholic metabolites of anthracycline, and cellular calcium homeostasis dysregulation cause chronic anthracycline cardiotoxicity. Recently, an important role for reactive nitric species and iron homeostasis deregulation was suspected. Some reactive oxygen and nitric species might react with one another to produce new, highly toxic products. It is suggested that after anthracycline administration, reactive oxygen and nitric species affect cellular calcium and iron homeostasis deregulation. The possible connection between reactive oxygen and nitric species and calcium and iron deregulation is presented in the paper.

Animals↗

PubMed2006

[The influence of hyperventilation in combination with active orthostasis on the condition of vegetative homeostasis in young men with atherosclerosis risk factors and endothelial dysfunction].

The aim of the study was to evaluate the effects of hyperventilation test (HVT), active orthostatic position test (AOPT), and their combination on the vegetative homeostasis in male students with risk factors of atherosclerosis (RFA) and endothelial dysfunction (ED). The mentioned tests and their combination were performed in 142 male students with RFA and ED, and 54 male students without them during brachial arterial rheovasography and cardiointervalography. Hyperactivation of the central regulatory circuit and a spastic hemodynamic condition at rest were found in subjects with FRA and ED. The sympathetic functional reserve was overstrained according to AOPT, distinctly decreased according to HVT, and exhausted when both tests were performed. The combination of HVT and AOPT is an informative stress test for pre-clinical evaluation of disturbances in adaptation mechanisms and vegetative homeostasis tensity in young men with RFA and ED. A "high value" of adaptation and the vegetative homeostasis overstrain in male students with FRA and ED indicate a premorbid condition in them.

Adolescent↗

PubMed1991

Bioelectrical homeostasis as a component of acupuncture mechanism.

Low frequency electrical current and super-high frequency electromagnetic field were applied to acupuncture points of stomach meridian in dogs. The stimulation effect on Bioelectrical potentials of 5 acupuncture points of stomach, spleen, liver, kidney, small intestine meridians and non-acupuncture skin zones was studied in conditions of blocked autonomic ganglia or neuro-muscular junctions of the dog. The influence of ganglioblockading and myorelaxating drugs on Bioelectrical potentials of acupuncture points was also researched. The results are discussed from the neurohumoural and bioelectrical hypotheses points of view. The conclusion that both mechanisms of acupuncture supplement each other is drawn. The principle of bioelectrical homeostasis as a component of acupuncture mechanism is proposed. Bioelectrical homeostasis along with other kinds of homeostasis forms a system of first level homeostats which is united into second level homeostat by the autonomic nervous system.

Animals↗

PubMed2006

[Comparative analysis of the influence of various factors in different combinations on the ionic homeostasis of a cell].

The ionic homeostasis is one of the most sensitive tests for the evaluation of functional state of a cell. The agents, which promote elevation of ionic homeostasis, as well as those, which suppress it, are well known. The goal of the present work was tracing the possibilities for altering ionic homeostasis into one or another direction, as a result of combined influence of some agents: ionizing radiation at a dose of 0.1 Gy, EMF with frequency of 45 Hz, 2.0 mT, in one case, and addition to this combination of the homeopathic remedy--stimulated phosphoric acid, at different dilutions. The following data have been obtained: combination of ionizing radiation of 0.1 Gy increased effect against the effect of its constituents, while addition of phosphoric acid at dilution of 10(-14) increased effect even further. In the other series of experiments, combination of ionizing radiation of 0.5 Gy and EMF was used in the same conditions; as a result, the sum effect decreased against its constituents, while addition of highly diluted (10(-200)) phosphoric acid practically arrested this effect. It is concluded that effect of a combined influence depends on a dose of the constituents.

Animals↗

PubMedDate not supplied

[A comparative assessment of homeostasis and hemodynamics during the performance of bicarbonate and acetate hemodialysis].

The article deals with the comparative analysis of certain values of homeostasis and hemodynamics in 25 patients with chronic renal failure who were subjected to systematic bicarbonate and acetate hemodialysis. Comparative study of some values of homeostasis, hemodynamics and myocardial contractility in patients with chronic renal failure during hemodialysis with acetate and bicarbonate solutions showed the advantages of bicarbonate hemodialysis. During bicarbonate hemodialysis, in addition to the patients' good tolerance to the procedure, the correction of the disturbed homeostasis was more physiological on the one hand, and positive shifts occurred in the activity of the blood circulatory system on the other. The study showed the expediency of using bicarbonate hemodialysis in patients with chronic renal failure with individual intolerance to acetate solution, and with severe heart failure and metabolic acidosis.

Acetates↗

PubMed1990

Experimental evidence for hypothalamic paraventricular nucleus involvement in the regulation of carbohydrate homeostasis.

An attempt was made to elucidate whether the hypothalamic paraventricular nucleus (PVN) is involved in carbohydrate homeostasis regulation in rats. The cellular responses to various disturbances of homeostasis were studied in the neuronal subdivisions (subnuclei) of the PVN. The responses were assessed in terms of changes in the sizes of the cell nuclei, nucleoli, and cytoplasm, and by the ultrastructural changes evident in cellular organelles. Significant cellular responses were observed in several subnuclei, with the nature of the responses being determined by the type of homeostatic alteration. The results indicate the possible involvement of the PVN subnuclei in the regulation of carbohydrate homeostasis.

Animals↗

PubMed1990

Altered calcium homeostasis in irreversibly injured P388D1 macrophages.

Sequestration of calcium by mitochondria is an important mechanism to maintain normal intracellular calcium homeostasis. Anoxic or toxic damage to these organelles has been postulated to disrupt intracellular calcium compartmentalization, leading to cell death. The authors examined the potential relationship between mitochondrial dysfunction, altered calcium homeostasis, and irreversible injury in a model system of silica-induced toxicity to P388D1 cells. Exposure to toxic silica particles, but not to nontoxic latex heads, disrupted mitochondrial membrane potential, increased membrane-associated calcium, elevated free cytosolic calcium, and killed 50% to 60% of the cell population after 6 to 8 hours. To test whether disruption of the mitochondrial membrane potential was sufficient to cause irreversible injury, P388D1 cells were exposed to either the proton ionophore, carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP) or to the mitochondrial inhibitor, antimycin A. Over 90% of the treated cells showed depolarization of the mitochondrial membrane as indicated by the fluorescent probe rhodamine 123. Carbonyl cyanide p-trifluoromethoxyphenylbydrazone also caused an elevation in free cytosolic calcium as monitored by fura-2. However, even after 6 hours of exposure to these proton ionophores or mitochondrial inhibitors, P388D1 cells did not show increased chlorotetracycline (CTC)-induced fluorescence or loss of viability. P388D1 cells exposed to silica have been shown previously to lose 80% of their adenosine triphosphate (ATP) content. The effect of reduced ATP levels on intracellular calcium homeostasis and viability was assessed by exposing P338D1 cells to FCCP in the presence of sodium azide and 2-deoxyglucose, which reduced ATP content by more than 90%. Under these conditions, none of the cells were killed, and only 5.5% showed increased CTC-induced fluorescence after 6 hours. These data indicate that disruption of the mitochondrial membrane potential, even in combination with reduced ATP content, is not sufficient to kill P388D1 cells.

Adenosine Triphosphate↗

PubMed1989

Important factors in the maintenance of homeostasis in the surgical patient.

Three factors that influence homeostasis are discussed: fluids and electrolytes, energy and nutrition, and immune response mediators. Cell injury induces changes in the sodium-potassium pump that disrupt fluid and electrolyte homeostasis, and surgery causes changes in functional extracellular fluid. Caloric requirements increase in proportion to the severity of the injury, and are generally greater than expected. Both parenteral and enteric feeding restore alanine and glutamine levels toward normal. Studies suggest that some of the adverse effects of surgery on homeostasis may be alleviated by specific treatments. A major key in modulating the stress response to surgery may lie in controlling immune response mediators, in particular cachectin, which has been shown to cause effects identical to those of septic shock. Recent studies have indicated that injections of small doses of specific monoclonal antibody to cachectin can avert all of the mediator's adverse effects.

Energy Intake↗

PubMed1987

[Homeostasis of plasma amino acids in standardized parenteral nutritional therapy in acute necrotizing pancreatitis].

The study investigates amino acid homeostasis and nitrogen balance in patients with acute necrotizing pancreatitis. 10 patients received a parenteral nutritional regimen containing 1 g of amino acids/kg B.W./day and 6.5 g of carbohydrates/kg B.W./day. Parameters to define homeostasis were measured to characterize the patients. In addition we determined the plasma amino acids and the nitrogen balance. All those biochemical parameters measured to define homeostasis remained within the physiological reference range. The description of the relative amino acid pattern only demonstrated changes of the postoperatively typically altered amino acids, e.g. phenylalanine.

Acute Disease↗