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PubMed1994

Calcium homeostasis in normal pregnancy and puerperium. A longitudinal study.

Calcium homeostasis was longitudinally followed in serum and urine throughout normal pregnancy and the puerperium in 23 healthy women. From the 14th week of gestation, samples were obtained every fourth week until the 38th week. Post partum samples were obtained on the fifth day and after eight weeks. In the serum the total calcium decreased continuously during pregnancy. The ionized calcium and phosphate levels remained unchanged and within the reference interval for non-pregnant women. The alkaline phosphatase level progressively increased and high levels were found at term. The magnesium and hematocrit values remained below, whereas the calcitonin level remained just above the reference interval throughout pregnancy. The parathyroid hormone was low initially and increased towards term but within the reference interval. The urine excretion of calcium was constantly high, close to the upper reference limit, and renal function was slightly improved. At the last sampling eight weeks after delivery, all values were within normal limits for non-pregnant women. Calcium homeostasis is considerably changed during pregnancy and non-pregnant reference limits are not often valid.

Adolescent↗

PubMedDate not supplied

Labyrinthine barriers and cochlear homeostasis.

The blood-labyrinth barrier is a concept used to explain the stability of composition of the labyrinthine fluids in spite of systemic alterations in blood composition. This blood-labyrinth barrier concept was tested by injecting various test substances into the systemic circulation of experimental animals and recovering these compounds in perilymph. The concentration of each test substance in perilymph lagged behind that of serum, and the transport of a series of test substances was found to be inversely related to the molecular weight and diameter. Among the osmotic agents injected, glycerol and urea penetrated into perilymph to a considerable degree, however, mannitol did not enter perilymph in any significant amount. This may explain the clinical differences noted with these agents in testing for Meniere's disease. Furosemide, an ototoxic diuretic, was found to penetrate into perilymph after intravenous injection into chinchillas. The concentration of furosemide, measured by high pressure liquid chromatography, was fairly constant at the time of full recovery of endocochlear potential after doses of 50-200 mg/kg. The principle of correlating drug concentration in serum and in inner ear fluids with pathophysiologic effect may provide a prediction of threshold concentration of ototoxic effect by measurement of serum concentration of the drug. More extensive studies are necessary to clarify the role of the blood-labyrinth barrier in the regulatory mechanisms which maintain the homeostasis in the inner ear and the pathology which may follow when this homeostasis is disrupted.

Biological Transport↗

PubMed1988

Imbalanced calcium homeostasis and endolymphatic hydrops.

In this paper the current state of knowledge of the development in experimental endolymphatic hydrops (EEH) is summarized, with particular emphasis on calcium. An imbalanced Ca2+ homeostasis in the inner ear is demonstrated using EEH as an animal model for Meniere's disease. The possibility of a receptor-mediated Ca2+ transport across the epithelial layer, especially the light cells, and of 'chemical signal' as an initiating modulating factor in the disturbance of Ca2+ homeostasis was suggested. It is pointed out that melanin is capable of binding calcium and may act as a buffering system. Finally, the possible malfunction of the Ca-overloaded melanocytes on the inner ear function is discussed.

Animals↗

PubMed1997

The ultradian clocks of eukaryotic microbes: timekeeping devices displaying a homeostasis of the period.

Temperature compensation of their period is one of the canonical characteristics of circadian rhythms, yet it is not restricted to circadian rhythms. This short review summarizes the evidence for ultradian rhythms, with periods from 1 minute to several hours, that likewise display a strict temperature compensation. They have been observed mostly in unicellular organisms in which their constancy of period at different temperatures, as well as under different growth conditions (e.g., medium type, carbon source), indicates a general homeostasis of the period. Up to eight different parameters, including cell division, cell motility, and energy metabolism, were observed to oscillate with the same periodicity and therefore appear to be under the control of the same central pacemaker. This suggests that these ultradian clocks should be considered as cellular timekeeping devices that in fast-growing cells take over temporal control of cellular functions controlled by the circadian clock in slow-growing or nongrowing cells. Being potential relatives of circadian clocks, these ultradian rhythms may serve as model systems in chronobiological research. Indeed, mutations have been found that affect both circadian and ultradian periods, indicating that the respective oscillators share some mechanistic features. In the haploid yeast Schizosaccharomyces pombe, a number of genes have been identified where mutation, deletion, or overexpression affect the ultradian clock. Since most of these genes play roles in cellular metabolism and signaling, and mutations have pleiotropic effects, it has to be assumed that the clock is deeply embedded in cellular physiology. It is therefore suggested that mechanisms ensuring temperature compensation and general homeostasis of period are to be sought in a wider context.

Acanthamoeba↗

PubMed2000

Do immune complexes formed with autoantibodies have a role in the maintenance of immune homeostasis through interaction with FC receptors.

Natural autoantibodies play an important regulatory role in the maintenance of immune homeostasis. They act as a first line of defense against environmental pathogens like toxins, bacteria and erythrocytes. In humans they are mainly produced by CD5+ B cells that are under the control of a regulatory T cell population. Fc-gamma receptors are involved in antigen recognition and signal transduction and tuning, and some of the members of the FcR family have structural similarity to MHC molecules; they may interact with multiple Ig ligands and with non-Ig ligands. We discuss the interactions between immune-complexes formed with natural autoantibodies and Fc-gamma receptors and suggest that such interactions may affect self-recognition in the thymus and regulate immune homeostasis.

Antigen-Antibody Complex↗

PubMedDate not supplied

Angiotensin as neuromodulator/neurotransmitter in central control of body fluid and electrolyte homeostasis.

Stimulation of central angiotensin receptors promotes, among others, drinking behaviour, stimulation of natriuresis and increased release of vasopressin. Angiotensin (ANG II)-containing pathways in the lamina terminalis and the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, brain areas involved in the regulation of body fluid homeostasis, have been described. All these areas express predominantly AT1 receptors. The drinking response and the vasopressin release to centrally administered ANG II are mediated by AT1 receptors, while AT2 receptors exert inhibitory effects. Evidence for the involvement of the catecholaminergic and angiotensinergic pathways in the PVN and SON in mediating the ANG II-induced release of vasopressin is presented. ANG II is released in the PVN upon local osmotic stimulation and water deprivation. Finally, we present evidence that activation of central angiotensinergic receptors, water deprivation, or hypertonicity induce transcription of immediate-early genes and expression of the respective proteins in the lamina terminalis and in the PVN and SON. The summarized data implicate ANG II as a neuromodulator/neurotransmitter in central control of body fluid and electrolyte homeostasis.

Angiotensin II↗

PubMed2005

Cerebral acid-base homeostasis after severe traumatic brain injury.

OBJECT: Brain tissue acidosis is known to mediate neuronal death. Therefore the authors measured the main parameters of cerebral acid-base homeostasis, as well as their interrelations, shortly after severe traumatic brain injury (TBI) in humans. METHODS: Brain tissue pH, PCO2, PO2, and/or lactate were measured in 151 patients with severe head injuries, by using a Neurotrend sensor and/or a microdialysis probe. Monitoring was started as soon as possible after the injury and continued for up to 4 days. During the 1st day following the trauma, the brain tissue pH was significantly lower, compared with later time points, in patients who died or remained in a persistent vegetative state. Six hours after the injury, brain tissue PCO2 was significantly higher in patients with a poor outcome compared with patients with a good outcome. Furthermore, significant elevations in cerebral concentrations of lactate were found during the 1st day after the injury, compared with later time points. These increases in lactate were typically more pronounced in patients with a poor outcome. Similar biochemical changes were observed during later hypoxic events. CONCLUSIONS: Severe human TBI profoundly disturbs cerebral acid-base homeostasis. The observed pH changes persist for the first 24 hours after the trauma. Brain tissue acidosis is associated with increased tissue PCO2 and lactate concentration; these pathobiochemical changes are more severe in patients who remain in a persistent vegetative state or die. Furthermore, increased brain tissue PCO2 (> 60 mm Hg) appears to be a useful clinical indicator of critical cerebral ischemia, especially when accompanied by increased lactate concentrations.

Acid-Base Equilibrium↗

PubMed2005

Involvement of amyloid beta precursor protein (AbetaPP) modulated copper homeostasis in Alzheimer's disease.

AbetaPP is involved in Cu homeostasis in mouse and man. In vitro observations and in vivo data obtained from AbetaPP mouse models at least provide strong evidence that AbetaPP and Abeta overproduction enables intracellular Cu to be transported out of the cell. The increased Cu efflux seems to lead to a Cu deficiency and a subsequently reduced SOD-1 activity. Studies have shown that a disturbed metal-ion homeostasis with elevated serum Cu levels occurs in Alzheimer and Down's patients and lowered levels in post-mortem AD brain. We conclude that bioavailable Cu has beneficial and specific effects in Alzheimer's disease transgenic mice, and suggest that our observation can be regarded as a proof-of-concept for a prophylactic approach to overcome the observed CNS Cu deficiency in the brain of Alzheimer's disease patients.

Alzheimer Disease↗

PubMed2026

Graded Mulberry Leaf Supplementation Shapes Gut Microbiota, Reprograms Intestinal Metabolism, and Maintains Intestinal Chemical-Immune Barrier Homeostasis in Amur Sturgeon: A Multi-Omics Study.

Mulberry leaf contains abundant phytochemicals with antioxidant and immunomodulatory activities. However, systematic insight into its dose-dependent regulatory effects on the intestinal health of Amur sturgeon remains limited. In the present study, multi-omics approaches, including 16S rRNA gene sequencing, untargeted metabolomics, transcriptomics, together with RT-qPCR, were applied to investigate graded dietary mulberry leaf supplementation in Acipenser schrenckii. Juvenile sturgeons were fed four experimental diets containing 0%, 2%, 4% and 6% mulberry leaf over a 10-week feeding trial. Dietary mulberry leaf caused no adverse impacts on growth performance or intestinal digestive capacity. Although the overall structure of the intestinal microbiota remained stable, beneficial bacterial taxa were enriched in a dose-dependent manner. Intestinal metabolism underwent hierarchical remodelling: low inclusion levels supported basal nutrient metabolism, medium inclusion strengthened antioxidant capacity, and high inclusion reprogrammed lipid metabolism and immune function. Mulberry leaf reinforced the intestinal chemical barrier by balancing redox homeostasis and reducing mucosal epithelial permeability. Moreover, intestinal immunity was modulated through three sequential phases: initial innate immune priming, B-cell homing, and the establishment of sustained immune tolerance. In conclusion, mulberry leaf maintains intestinal chemical-immune barrier homeostasis in a dosage-tunable manner, supporting its potential application as a functional aquafeed ingredient.

Amur sturgeon (Acipenser schrenckii)↗

PubMed2026

Molecular and Physiological Insights into CAT- and SOD-Associated Redox Homeostasis Under Salt Stress in Artemisia argyi.

Soil salinity disrupts redox homeostasis and limits plant growth and development. Although catalase (CAT) and superoxide dismutase (SOD) are key enzymatic antioxidants, the CAT and SOD gene families have not been characterized in Artemisia argyi (A. argyi), a species of medicinal and ecological importance. While SOD and CAT serve as the primary enzymatic scavengers for reactive oxygen species (ROS) detoxification, their genomic architecture and stress-responsive regulatory networks in A. argyi have remained uncharacterized. In this study, we conducted the first comprehensive genome-wide analysis of these gene families in A. argyi, identifying 22 structurally conserved members (8 AarCATs and 14 AarSODs). Collinearity and synteny analyses revealed strict lineage-specific evolutionary conservation, while tertiary protein modeling and subcellular localization illustrated a highly organized multi-organelle defense compartmentalization. High salinity (up to 200 mM NaCl) reduced the stomatal conductance and net photosynthetic rate. Salt stress reduced growth and increased osmoprotectant and antioxidant accumulation in A. argyi. Furthermore, histochemical staining using nitroblue tetrazolium (NBT) and 3,3'-Diaminobenzidine (DAB) provided comprehensive evidence of significant accumulation of ROS in leaves, which indicates the intense oxidative stress triggered by ionic stress. Tissue-specific analysis revealed that AarCAT1, AarCSD1, and AarFSD2 were 3.9-, 7.9-, and 12.7-fold higher in leaves than in roots, respectively. Under stress, AarCAT6 and AarCSD1 were strongly repressed in leaves by ~50% and ~46-70%, respectively, whereas AarMSD2 and AarMSD3 were significantly induced in roots by ~2.2- and ~1.8-fold. These distinct expression patterns suggest their potential involvement in tissue-specific stress adaptation and ROS homeostasis. These findings uncover the evolutionary and physiological basis of salt tolerance in A. argyi, providing genetic targets for climate-resilient breeding.

Artemisia↗

PubMed2005

Expression profiling suggests a regulatory role of gallbladder in lipid homeostasis.

AIM: To examine expression profile of gallbladder using microarray and to investigate the role of gallbladder in lipid homeostasis. METHODS: 33P-labelled cDNA derived from total RNA of gallbladder tissue was hybridized to a cDNA array representing 17,000 cDNA clusters. Genes with intensities > or =2 and variation <0.33 between two samples were considered as positive signals with subtraction of background chosen from an area where no cDNA was spotted. The average gray level of two gallbladders was adopted to analyze its bioinformatics. Identified target genes were confirmed by touch-down polymerase chain reaction and sequencing. RESULTS: A total of 11 047 genes expressed in normal gallbladder, which was more than that predicted by another author, and the first 10 genes highly expressed (high gray level in hybridization image), e.g. ARPC5 (2 225.88+/-90.46), LOC55972 (2 220.32+/-446.51) and SLC20A2 (1 865.21+/-98.02), were related to the function of smooth muscle contraction and material transport. Meanwhile, 149 lipid-related genes were expressed in the gallbladder, 89 of which were first identified (with gray level in hybridization image), e.g. FASN (11.42+/-2.62), APOD (92.61+/-8.90) and CYP21A2 (246.11+/-42.36), and they were involved in each step of lipid metabolism pathway. In addition, 19 of those 149 genes were gallstone candidate susceptibility genes (with gray level in hybridization image), e.g. HMGCR (10.98+/-0.31), NPC1 (34.88+/-12.12) and NR1H4 (16.8+/-0.65), which were previously thought to be expressed in the liver and/or intestine tissue only. CONCLUSION: Gallbladder expresses 11 047 genes and takes part in lipid homeostasis.

Adult↗

PubMed2000

Normal lymphoid homeostasis and lack of lethal autoimmunity in mice containing mature T cells with severely impaired IL-2 receptors.

The importance of IL-2Rbeta function for immune regulation is highlighted by the severe impairment in lymphoid cell function in IL-2Rbeta-deficient mice. It has been speculated that failed IL-2/IL-2R signaling in peripheral T cells causes the associated autoimmunity, imbalanced peripheral lymphoid homeostasis, and defective T cell function. This study explored the requirement for IL-2Rbeta function in mature T lymphocytes. We show that transgenic thymic expression of the IL-2R beta-chain in IL-2Rbeta-deficient mice prevents lethal autoimmunity, restores normal production of B lymphocytes, and results in a peripheral T cell compartment that is responsive to triggering through the TCR, but not the IL-2R. The dysfunction of the IL-2R is illustrated by the near complete failure of mature T cells to proliferate to IL-2 in vitro and in vivo, to differentiate into CTL, and to up-regulate IL-2Ralpha expression. These data indicate that lymphoid homeostasis is largely maintained despite a nonfunctional IL-2R in mature T lymphocytes and suggest that IL-2Rbeta provides an essential signal during thymic development to regulate self-reactivity.

Animals↗

PubMed2000

The role of B7 costimulation in CD4/CD8 T cell homeostasis.

The effect of B7-mediated costimulation on T cell homeostasis was examined in studies of B7-1 (CD80) and B7-2 (CD86) transgenic as well as B7-deficient mice. B7 overexpression in transgenic mice resulted in marked polyclonal peripheral T cell hyperplasia accompanied by skewing toward an increased proportion of CD8 single-positive cells and a decreased proportion of CD4 single-positive cells in thymus and more markedly in peripheral T cells. B7-induced T cell expansion was dependent on both CD28 and TCR expression. Transgenic overexpression of B7-1 or B7-2 resulted in down-regulation of cell surface CD28 on thymocytes and peripheral T cells through a mechanism mediated by intercellular interaction. Mice deficient in B7-1 and B7-2 exhibited changes that were the reciprocal of those observed in B7-overexpressing transgenics: a marked increase in the CD4/CD8 ratio in peripheral T cells and an increase in cell surface CD28 in thymus and peripheral T cells. These reciprocal effects of genetically engineered increase or decrease in B7 expression indicate that B7 costimulation plays a physiological role in the regulation of CD4+ and CD8+ T cell homeostasis.

Abatacept↗

PubMed2001

Cutting edge: two distinct mechanisms lead to impaired T cell homeostasis in Janus kinase 3- and CTLA-4-deficient mice.

Cytokine receptor signaling and costimulatory receptor signaling play distinct roles in T cell activation. Nonetheless, deficiencies in either of these pathways lead to seemingly similar phenotypes of impaired T cell homeostasis. A dramatic expansion of CD4(+) peripheral T cells with an activated phenotype has been observed in both Janus kinase (Jak) 3-deficient and CTLA-4-deficient mice. Despite these similarities, the mechanisms driving T cell expansion may be distinct. To address this possibility, we examined the TCR repertoire of peripheral T cells in Jak3(-/-) and CTLA-4(-/-) mice using complementarity-determining region 3 spectratype analysis. Interestingly, a restricted and highly biased TCR repertoire was observed in the Jak3(-/-) T cells, strongly supporting a role for foreign Ag in the activation and expansion of these cells. In contrast, CTLA-4(-/-) T cells had a diverse and unbiased TCR repertoire, suggestive of a universal, Ag-independent mechanism of activation and expansion. These findings provide insight into the diverse mechanisms controlling T cell homeostasis.

Abatacept↗

PubMed2001

Expression of active protein kinase B in T cells perturbs both T and B cell homeostasis and promotes inflammation.

The molecular mechanisms that contribute to autoimmunity remain poorly defined. While inflammation is considered to be one of the major checkpoints in autoimmune disease progression, very little is known about the initiating events that trigger inflammation. We have studied transgenic mice expressing the prosurvival molecule protein kinase B/Akt under control of a T cell-specific CD2 promoter. In this study, we demonstrate that aged mice develop lymphadenopathy and splenomegaly that result from an accumulation of CD4, CD8, and unexpectedly B cells. An increased proportion of T cells express activation markers, while T cell proliferative responses remain normal. B cells are hyperproliferative in response to anti-IgM F(ab')(2) and anti-CD40, and increased IgA and IgG2a were found in the sera. In addition, a profound multiorgan lymphocytic infiltration is observed, and T cells from these mice display a defect in Fas-mediated apoptosis, which may be the mechanism underlying this phenotype. Therefore, T cell expression of active protein kinase B can alter T cell homeostasis, indirectly influence B cell homeostasis, and promote inflammation in vivo.

Animals↗

PubMed2001

Apoptosis and altered dendritic cell homeostasis in lupus nephritis are limited by anti-CD154 treatment.

Autoimmunity results from a failure in central and/or peripheral tolerance; however, the events that initiate and maintain this dysfunction remain unclear. To better understand the mediators involved in autoimmunity, we investigated the cellular mechanisms maintaining disease in the (SWR x NZB)F(1) (SNF(1)) mouse model of systemic lupus erythematosus. Previously, we have shown that autoimmunity in this model is dependent on CD40-CD154 interactions. Herein, our studies reveal that the severity of disease in SNF(1) mice correlates with a marked increase in the frequency of apoptotic splenocytes, including a higher proportion of apoptotic dendritic cells (DC) in vivo. In addition, we demonstrate a significant disease-related increase in the absolute number of splenic CD11c(high) DC. The increased DC number appears to be attributable to DC proliferation and enhanced migration to the spleen, most likely induced by elevated splenic expression of secondary lymphoid chemokine. Importantly, these imbalances in apoptosis, secondary lymphoid chemokine expression, and DC homeostasis were reduced or normalized by anti-CD154 treatment. Thus, our data demonstrate CD154-dependent regulation of apoptosis and DC homeostasis in mice with lupus-like autoimmune disease. We suggest that these mechanisms comprise an autostimulatory loop, maintaining the cascade of autoimmunity by DC presentation of self-Ags derived from apoptotic cells and CD154-mediated costimulation.

Animals↗

PubMed2002

Roles of SLC/CCL21 and CCR7 in human kidney for mesangial proliferation, migration, apoptosis, and tissue homeostasis.

The release of chemokines by intrinsic renal cells is an important mechanism for the regulation of leukocyte trafficking during renal inflammation. The expression of chemokine receptors by intrinsic renal cells such as mesangial cells (MC) suggests an expanded role for chemokine-chemokine receptor biology in local immunomodulation and potentially glomerular homeostasis. By immunohistochemistry we found the chemokine receptor CCR7 expressed in a mesangial pattern while the CCR7 ligand SLC/CCL21 showed a podocyte-specific expression. CCR7 expression was further characterized by RT-PCR, RNase protection assays, and FACS analysis of cultured human MC, and was found to be constitutively present. Real-time PCR of microdissected glomeruli confirmed the expression of SLC/CCL21. A functional role for CCR7 was demonstrated for human MC migration and proliferation. A protective effect of SLC/CCL21 was shown for MC survival in Fas Ab-induced apoptosis. Finally, "wound healing" was enhanced in the presence of SLC/CCL21 in an in vitro injury model. The constitutive glomerular expression of CCR7 and its ligand SLC/CCL21 in adjacent cell types of the human kidney suggests novel biological functions of this chemokine/chemokine receptor pair and a potential role in processes involved in glomerular homeostasis and regeneration.

Apoptosis↗

PubMed2002

Homeostasis of peripheral CD4+ T cells: IL-2R alpha and IL-2 shape a population of regulatory cells that controls CD4+ T cell numbers.

We show that the lymphoid hyperplasia observed in IL-2Ralpha- and IL-2-deficient mice is due to the lack of a population of regulatory cells essential for CD4 T cell homeostasis. In chimeras reconstituted with bone marrow cells from IL-2Ralpha-deficient donors, restitution of a population of CD25(+)CD4(+) T cells prevents the chaotic accumulation of lymphoid cells, and rescues the mice from autoimmune disease and death. The reintroduction of IL-2-producing cells in IL-2-deficient chimeras establishes a population of CD25(+)CD4(+) T cells, and restores the peripheral lymphoid compartments to normal. The CD25(+)CD4(+) T cells regulated selectively the number of naive CD4(+) T cells transferred into T cell-deficient hosts. The CD25(+)CD4(+)/naive CD4 T cell ratio and the sequence of cell transfer determines the homeostatic plateau of CD4(+) T cells. Overall, our findings demonstrate that IL-2Ralpha is an absolute requirement for the development of the regulatory CD25(+)CD4(+) T cells that control peripheral CD4 T cell homeostasis, while IL-2 is required for establishing a sizeable population of these cells in the peripheral pools.

Adjuvants, Immunologic↗