Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HOMEOSTASIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

The dynamics of quantifiable homeostasis. V: Homeostasis of higher order.

The properties are explored of a cybernetic process with lag L and force of restoration equal to the size of displacement one lag unit earlier, raised to any arbitrary positive power (w greater than 1), multiplied by the restoration constant b, the sign being opposite to that of the displacement at that time. No closed-form solution is available, but a converging Taylor series expansion is presented that gives a solution of arbitrary precision. Unlike the linear system previously discussed, the amplitude of the displacement (A) is germane, and it is shown that the criterion that the effect of a perturbation be damped out is whether or not LbAw-1 exceeds a constant, kw, that depends only on w. The counterpart of this pattern of higher-order homeostasis is closer to the biological behavior of many forms of homeostasis than the scaled invariance characteristic of the linear process. kw is shown to be bounded between pi/2 and 2, and increases monotonically with w. Exactly computed values and large-sample approximations are given for the critical values below which no overshoot at all occurs. It is shown that where it does not, the minimum expected cost decreases with increasing w and reaches a minimum at infinite w. However, this evolutionary gain is vitiated where large displacements are involved, and may need to be redressed by a change in the restoration constant. Thus, the dynamic balance becomes much more subtle than with lower-order processes. Several brief clinical illustrations of these ideas are presented.

Biological Evolution↗

Homeostasis--the key concept to physiological control. Surgery, stress and metabolic homeostasis.

In this series of articles we have illustrated how physiological processes enable adaptation to changing situations such as those associated with surgery. Homeostasis has formed the central theme for relating physiology to well being, and the articles have largely been concerned with the homeostatic regulation of specific systems or processes within the body (a list of articles in the series is provided at the end of this one). This final article maintains the theme but is concerned with the broader, whole-body responses that occur when the body is subjected to the trauma of surgery. Some of these responses have briefly been touched upon in earlier articles, but are expanded upon here to illustrate the adaptability of metabolic homeostasis when the body has been injured.

Energy Metabolism↗

Systematic mining and characterization of metal transporter families regulating zinc homeostasis provide insights into metal homeostasis in Camellia sinensis.

BACKGROUND AND AIMS: Zinc is essential for tea plant growth and quality formation, yet its homeostatic mechanisms remain poorly understood. This study identified metal transporter families regulating zinc homeostasis, analyzed their evolution, structure, and expression, and clarified zinc uptake, transport, detoxification networks, and their links to metabolism. METHODS: This study identified zinc homeostasis-related metal transporter families in the tea plant genome, characterized their structural features and expression profiles across tissues and developmental stages through integrative bioinformatics and transcriptomic analyses, and delineated the molecular mechanisms underlying zinc uptake, translocation, and detoxification by systematically integrating published evidence. RESULTS: This study identified 74 metal transporter genes from six families: 13 CsZIPs, 12 CsNRAMPs, 10 CsHMAs, 10 CsYSLs, 14 CsMTPs, and 15 CsCAXs in the 'Shuchazao2' genome, revealing closer affinity to woody species than to Arabidopsis. These proteins exhibit conserved domains, diverse subcellular localizations (cell membrane, vacuole, chloroplast, and Golgi apparatus), and tissue-specific expression with abundant stress/hormone-responsive cis-elements. At the plant-soil interface, tea plants mobilize rhizospheric zinc via proton and organic acid secretion; CsYSLs, CsNRAMPs, and CsZIPs mediate zinc uptake, aided by arbuscular mycorrhizal fungi (AMF) and plant growth-promoting rhizobacteria (PGPR) that expand root absorption zones. Xylem CsHMAs and phloem CsYSLs coordinate root-to-shoot zinc translocation, and vacuolar transporters (CsMTPs, CsCAXs), cell wall immobilization, and antioxidant systems alleviate high-zinc stress injury. CONCLUSIONS: These findings collectively delineate an integrated zinc "acquisition-distribution-buffering" network in tea plants, offering a repertoire of candidate genes with potential utility in zinc biofortification breeding and improving acid soil adaptation. Further experimental validation, including tea transgenesis, zinc-stress qRT-PCR, and heterologous functional complementation, is essential to substantiate their biological roles.

Camellia sinensis↗

The dynamics of quantifiable homeostasis. IV: Zero-order homeostasis.

A zero-order homeostatic process is one in which the corrective force a has sign opposite to that of what the displacement from the homing value was one lag (L) time earlier, but is unrelated to magnitude of displacement. The properties of a zero-order process are considered in some detail. Its stable state is an oscillation with a period of 4L and a maximum amplitude of aL. It is suggested that this property is exploited in evolution for intrinsically rhythmical processes, and several examples (respiration, menstruation, and heart beat) are discussed. The parameters may be modulated by an ancillary cybernetic (retreat) circuit and hence the properties of the oscillation controlled as need be. Zero-order oscillation has means of conserving information through phase shifts. Also, when it is combined with a linear cybernetic process (with restoration constant b), it prevents information in the latter from dying out, even if Lb is less than pi/2 (which in a pure linear process would ensure extinction of all signs of perturbation). A further elaboration is the Dilman process of zero order in which there is a threshold of displacement below which homeostatic responses are not evoked. The merits of the value of the threshold are discussed. The properties of the zero-order process with a first-order retreat function furnish a tentative explanation for why hormonal homeostasis does not operate directly through the pituitary but involves the hypothalamus and intermediate hormone-releasing factors.

Blood Pressure↗

The statistics of quantifiable homeostasis. I. Simple linear homeostasis.

The statistical properties are explored of the least-squares estimators of the parameters of a deterministic linear model for homeostasis with random, normally distributed technical errors. The parameters are: the amplitude of perturbation (A), the homing value (H), the restoration constant (B), and the lag time (L). The former two, although important in their own right, tell us nothing about the processes of biologic restitution and are thus considered "nuisance" parameters; the latter two are the "business" parameters, which tell us about the processes of biologic adjustment. The properties studied include bias and precision and their relationships to the number of data points and to the size of the technical error. Efforts have been concentrated on data points equally spaced over six lag times (which corresponds roughly to the period of observation used in loading studies, such as glucose tolerance tests). The distributions of these four estimators are studied in sets of 100 Monte Carlo simulations, each with 15, 30, and 100 data points, respectively. The estimators are virtually unbiased and all satisfactorily close to Gaussian. The residual mean-square errors (the divisor being four less than the number of data points, since four parameters are estimated) seem to be unbiased estimators of the variances of the errors. Moreover, when suitably scaled, the residual sums of squares have distributions close to the chi-square distribution for the appropriate degrees of freedom and with the corresponding means and variances. The correlations among the estimators are modest and, except where A is involved, small.

Homeostasis↗

Interrelationship of dietary Mg intake and electrolyte homeostasis in hamsters: I. Severe Mg deficiency, electrolyte homeostasis, and myocardial necrosis.

Epidemiological studies indicate a strong relationship between dietary Mg intake and the incidence of sudden cardiac death. The mechanism by which dietary Mg leads to an increased incidence of cardiovascular disease is unknown but may involve alteration of electrolyte balance. In the present study, tissue electrolyte levels and myocardial pathology were investigated in adult hamsters fed a diet containing no added Mg. Control animals were fed the same diet supplemented with Mg or standard laboratory chow. Hamsters were killed after 4, 8, 12, or 18 days on the test diet, and levels of Na, K, Ca, and Mg were measured in the serum, myocardium, bone, and kidney. The earliest change induced by the test diet was a decrease of the serum Mg and an increase in the Na concentration of the myocardium and other tissues. Following the rise in myocardial Na, the myocardial Ca rose, attaining a fourfold increase by 18 days. K fell in heart and kidney, but not significantly. Although there was no significant change in myocardial Mg, foci of myocardial necrosis, considered to be typical of acute severe Mg deficiency, were found. Myocardial necrosis and the increase in myocardial Ca occurred in parallel. Because of the pattern of observed changes in electrolyte levels, and the potential role of Ca in myocardial injury, the occurrence of myocardial necrosis in these Mg-deficient hamsters is attributable to the increased level of myocardial Ca, rather than to any change in intracellular Mg levels. It is postulated that reduced extracellular Mg levels increase [Na]i through reduction of sarcolemmal (Na+ + K+)-ATPase activity. This would lead to an increase in [Ca]i through Na-Ca exchange.

Acid-Base Equilibrium↗

[Glucose homeostasis. II. Homeostasis disturbances--hypoglycemia in newborns and infants].

Since glucose is a vital fuel for the brain, hypoglycaemia demands prompt recognition, effective treatment, and accurate identification of the cause. However, pointing the cause, especially in children, can be and often is difficult. Neonatal hypoglycaemia is of a particular importance for paediatricians, since it is, when prolonged or recurrent, a preventable cause of mental retardation and permanent neurological damage. Neonatal hypoglycaemia can be transient or persistent and both of these groups can be further subdivided into two subgroups, where the aetiology of hypoglycaemia is primarily due to decreased hepatic glucose production or to increased peripheral glucose utilization. This article describes first part of causes of neonatal hypoglycaemia.

Adult↗

Ethanol effects on cultured embryonic hippocampal neuronal calcium homeostasis are altered by nerve growth factor.

The neurotoxic effect of acute ethanol treatment (AET) may lead to an alteration in the regulation of calcium (Ca2+) homeostasis in hippocampal neurons. Ca2+ homeostasis could be affected by AET when neurons are at rest or after depolarizing activity during synaptic transmission. It has been shown that nerve growth factor (NGF) can ameloriate some types of neurotoxicity by stabilizing Ca2+ homeostasis. Previously, we observed that ethanol (EtOH) changed unstimulated (basal) and potassium (K+)-stimulated intracellular calcium ([Ca2+]i) in embryonic septohippocampal neurons (Webb et al., Brain Res. 729:176-189, 1996). The purpose of the present study is to determine the effects of NGF and EtOH on neuronal Ca2+ homeostasis in cultured embryonic hippocampal neurons. The hypotheses tested were the following: EtOH alters Ca2+ homeostasis in hippocampal neurons; NGF modulates Ca2+ homeostasis in hippocampal neurons; and NGF treatment alters the effect of EtOH on [Ca2+]i in hippocampal neurons. Our results indicated that hippocampal neuronal cultures treated with EtOH had lower basal [Ca2+]i than untreated neurons. EtOH decreased K+-stimulated (30 mM KCI) changes in [Ca2+]i in a dose-dependent manner. During K+ stimulation, 20 ng/ml of NGF slowed and reduced the increase in [Ca2+]i. Hippocampal neurons treated with NGF increased or did not change basal [Ca2+]i and did not change or increase K+-stimulated [Ca2+]i in response to EtOH. These responses were dose-related and indicated that NGF could alter the response of hippocampal neurons to EtOH. In conclusion, AET results in the alteration of Ca2+ homeostasis in unstimulated and depolarized cultured embryonic hippocampal neurons. NGF and EtOH independently and collectively affected the regulation of Ca2+ homeostasis in this neuronal population. Changes in [Ca2+]i can disrupt normal cellular function and contribute to cell death. Therefore, alteration of Ca2+ homeostasis may be an underlying mechanism involved in EtOH toxicity. NGF may ameliorate the toxic effects of EtOH by regulating Ca2+ homeostasis.

Animals↗

Measuring frailty in the hospitalized elderly: concept of functional homeostasis.

Functional homeostasis is the ability of an individual to withstand illness without loss of function. We investigate whether the level of functional homeostasis predicts adverse outcomes in the 6 months posthospital discharge in older men and women. A prospective cohort study was conducted in an acute care geriatric inpatient unit of a university hospital. Subjects included a consecutive series of patients admitted to the unit. The Functional Independence Measure (FIM) instrument was used to assess patients at four time points: preillness, hospital admission, hospital discharge, and 6 months postdischarge. Of the 122 subjects available for analysis, 64 (52%) experienced a decline in functional level from preillness to hospital discharge and were defined as having poor functional homeostasis, whereas 58 (48%) experienced no change or an increase in functional status and were defined as having good functional homeostasis. Those with poor functional homeostasis had a higher 6-month readmission rate to the hospital (59.4 v 39.7%; P=0.03) and a higher rate of any adverse outcome (78.1 v 50%; P=0.001) than those with good functional homeostasis. In logistic regressive analyses, functional homeostasis remained a significant and powerful predictor of adverse outcomes independent of actual level of function at discharge, age, gender, living status, and other factors that might influence outcomes. Change in functional status associated with an acute illness is an independent predictor of adverse outcomes and, in this study, a better predictor than actual level of function at discharge. Functional homeostasis is one approach to the quantification of the important but elusive concept of frailty in the elderly.

Activities of Daily Living↗

Acupuncture and homeostasis: physiological, physical (postural) and psychological.

When the subject of homeostasis is discussed, one automatically thinks of physiological homeostasis, in particular such things as fluid and electrolyte balance, and the maintenance of body temperature, blood pressure and blood sugar, etc. In fact, two other concepts of homeostasis exist in the literature, namely physical or postural homeostasis, and also psychological homeostasis. The former applies to the situation where the line of gravity of the body in the erect posture passes in the frontal or coronal plane directly through the center of the axis of the atlanto-occipital, shoulder, hip, knee and ankle joints. Only a very small proportion of people attain this ideal balanced posture. Psychological homeostasis refers to emotional control or tranquility. It has been stated that the biological function of human emotion is primarily homeostatic. Repression is a homeostatic mechanism. Evidence is presented to show that a feedback type of relationship probably exists between these forms of homeostasis, and any of the body-mind type of therapies (including acupuncture and T'ai chi ch'uan) thus have a three-fold effect on man, i.e. on his physiology, his posture and his mind.

Acupuncture Therapy↗

Lead intoxication alters basal and parathyroid hormone-regulated cellular calcium homeostasis in rat osteosarcoma (ROS 17/2.8) cells.

The skeleton is the major reservoir of lead and calcium in humans, and plays an important role in systemic calcium regulation. Lead perturbs normal calcium transport and second messenger function, directly or indirectly, in virtually all cells studies so far. Therefore, we and others have postulated that an early and discrete toxic effect of lead is perturbation of one or more loci within the calcium messenger system. To understand further the role of lead on calcium homeostasis in bone, we undertook this study to characterize calcium homeostasis and the effect of lead on calcium homeostasis in rat osteosarcoma (ROS 17/2.8) cells, which exhibit the osteoblast phenotype. ROS cells were incubated in medium containing 45Ca for 20 hours. Monitoring the efflux of 45Ca from the cultures for 210 minutes allowed for the determination of kinetic parameters defining steady state calcium homeostasis. Three distinct intracellular kinetic calcium pools characterized 45Ca homeostasis. Treatment with either 400 ng parathyroid hormone (PTH)/ml culture medium for 1 hour or 25 microM lead for 20 hours increased total cell calcium. Treatment with PTH caused a larger increase of cell calcium in lead-intoxicated cells than either lead intoxication or PTH treatment alone. This increase suggests that lead may perturb normal calcium-mediated PTH responsiveness of the osteoblast. These experiments further establish a kinetic model for the study of calcium homeostasis in osteoblastic bone cells. The studies also advance the hypothesis that lead-induced perturbations of calcium-mediated processes represent an early effect of lead toxicity at the cellular level.

Animals↗