IN VIVO AND IN VITRO STUDIES ON IONIZED VERSUS TOTAL SERUM CALCIUM IN HYPERPARATHYROIDISM

1973 ◽  
Vol 74 (3) ◽  
pp. 501-510 ◽  
Author(s):  
F. Lindgärde
Keyword(s):  
Calcium Binding ◽  
Binding Capacity ◽  
Total Serum ◽  
Total Serum Calcium ◽  
Point Of Intersection ◽  
Straight Lines ◽  
And Control ◽  
The Relationship

ABSTRACT Measurements of ionized (Ca+ + ) calcium and total (Cat) calcium have been performed in sera from hyperparathyroid, parathyroidectomized and control subjects. The relationship between Ca++ and Cat has been analysed statistically. It was found that two straight lines with the point of intersection at Ca++ =2.75 and Cat = 5.55 mEq./l, and slopes of 0.628 and 0.447, respectively, would describe the data more accurately than one single line. However, when the calcium level was varied by the addition of calcium chloride in vitro in individual or pooled sera, the Ca++–Cat relationship appeared to be linear. The results suggest that sera from hyperparathyroid subjects have an increased calcium binding capacity.

Activity-Related Calcium Dynamics in Motoneurons of the Nucleus Hypoglossus From Mouse

1999 ◽  
Vol 82 (6) ◽  
pp. 2936-2946 ◽  
Author(s):  
Mario B. Lips ◽  
Bernhard U. Keller
Keyword(s):  
Quantitative Analysis ◽  
Action Potential ◽  
Calcium Binding ◽  
Calcium Influx ◽  
Binding Capacity ◽  
Calcium Transients ◽  
Calcium Dynamics ◽  
The Brain

A quantitative analysis of activity-related calcium dynamics was performed in motoneurons of the nucleus hypoglossus in the brain stem slice preparation from mouse by simultaneous patch-clamp and microfluorometric calcium measurements. Motoneurons were analyzed under in vitro conditions that kept them in a functionally intact state represented by rhythmic, inspiratory-related bursts of excitatory postsynaptic currents and associated action potential discharges. Bursts of electrical activity were paralleled by somatic calcium transients resulting from calcium influx through voltage-activated calcium channels, where each action potential accounted for a calcium-mediated charge influx around 2 pC into the somatic compartment. Under in vivo conditions, rhythmic-respiratory activity in young mice occurred at frequencies up to 5 Hz, demonstrating the necessity for rapid calcium elevation and recovery in respiratory-related neurons. The quantitative analysis of hypoglossal calcium homeostasis identified an average extrusion rate, but an exceptionally low endogenous calcium binding capacity as cellular parameters accounting for rapid calcium signaling. Our results suggest that dynamics of somatic calcium transients 1) define an upper limit for the maximum frequency of respiratory-related burst discharges and 2) represent a potentially dangerous determinant of intracellular calcium profiles during pathophysiological and/or excitotoxic conditions.

A bone matrix calcification-initiator noncollagenous protein

1977 ◽  
Vol 232 (3) ◽  
pp. C115-C127 ◽  
Author(s):  
M. R. Urist ◽  
A. J. Mikulski ◽  
M. Nakagawa ◽  
K. Yen
Keyword(s):  
Calcium Binding ◽  
Binding Capacity ◽  
Bone Matrix ◽  
Bone Collagen ◽  
Chemical Extraction ◽  
Insoluble Residue ◽  
Affinity Constant ◽  
Sequential Chemical Extraction

When completely demineralized, the densely packed structure of bone matrix does not recalcify, neither in physiologic solutions in vitro nor in implants in vivo. Even when inorganic and organic calcification inhibitors (which normally are stored in bone matrix) are removed first by autolytic digestion in neutral buffers at 37C and then by sequential chemical extraction, implants of the EDTA insoluble residue will not recalcify after as long as 4 wk in a muscle pouch. However, if first demineralized in cold dilute HCl, second, extracted and autodigested in buffers solution at 37C, and then further extracted in EDTA and other solutions at 2C, a calcification initiator protein (Cp) is unmasked, and the residue will invariable recalcify. CIP, isolated by gel filtration and column chromatography, is a disulfide-bonded glycoprotein aggregate composed of subunites of a moleclar mass of 55,000. CIP is composed of a large proportion of acidic amino acids and has a calcium binding capacity of about 1.8 times greater than albumin. The affinity constant CaCIP, calculated by ultrafiltration of physiologic solutions of Ca2+, is log K, 2.9. Observations on implants of residues that containe a) CIP but not a bone morphogenetic property (BMP), B) BMP accompanied by CIP activity, or c) neither BMP nor CIP activity suggested that BMP covers CIP and that the two are attached to bone collagen in tandem. Whether CIP plays a part in calcification of the normal skeleton requires further investigation.

scholarly journals Promoting the Calcium-Uptake Bioactivity of Casein Phosphopeptides in vitro and in vivo

2021 ◽  
Vol 8 ◽  
Author(s):  
Guo Liu ◽  
Baoyan Guo ◽  
Shengwei Sun ◽  
Minna Luo ◽  
Fei Liu ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Calcium Transport ◽  
Calcium Uptake ◽  
Calcium Absorption ◽  
Serum Alkaline Phosphatase ◽  
Binding Capacity ◽  
Animal Experiments ◽  
Casein Phosphopeptides

Casein phosphopeptides have been studied widely for their ability to chelate calcium. However, systematic studies on the effects of casein phosphopeptides (CPP) on calcium absorption in vitro and in vivo are scarce. The purities of two commercially available products, CPP1 and CPP2, are 18.37 and 25.12%, respectively. Here, the in vitro calcium binding capacity of CPP2 was 142.56 ± 7.39 mg/g, which was higher than that of CPP1 (107.15 ± 6.27 mg/g). The calcium transport results in a Caco-2 monolayer model indicated that, relative to controls, CPP1 and CPP2 increased calcium transport by 21.78 and 53.68%, respectively. Subsequent animal experiments showed that the CPP2-Ca-H group (1% Ca, 0.4% CPP2) had significant increases in the femur index, serum Ca2+ and serum osteocalcin levels, and femoral Ca content. The CPP2-Ca-H animal also had decreased serum alkaline phosphatase levels, parathyroid hormone content, and urinary pyridinoline content. Overall, our results demonstrated that CPP2 had stronger effects on promoting calcium uptake than CPP1.

Age-related changes in composition and Ca2+-binding capacity of canine cortical bone extracts

1988 ◽  
Vol 255 (1) ◽  
pp. H101-H110 ◽  
Author(s):  
M. R. Pinto ◽  
J. P. Gorski ◽  
J. T. Penniston ◽  
P. J. Kelly
Keyword(s):  
Calcium Binding ◽  
Organic Phosphorus ◽  
Binding Capacity ◽  
Exchange Process ◽  
Age Groups ◽  
Binding Studies ◽  
Exchangeable Calcium ◽  
Age Related

The variable of age was used to study macromolecules in bone that may mediate in part the in vivo readily exchangeable calcium-binding capacity (VCa2+D). Organic components were extracted from nonmineralized bone with 4 M guanidine-HCl and from both nonmineralized and mineralized bone with 0.1 M EDTA. The composition of pup bone extracts demonstrated an enrichment in protein, hexuronate, sialic acid, organic phosphorus, and bound sulfate when compared with other age groups. In vitro calcium-binding studies identified low-affinity (Kd congruent to 10(-3) M) sites in both types of extracts; high-affinity sites (Kd congruent to 10(-5) M) were only evident in EDTA extracts of bone. Readily exchangeable calcium-binding capacity in vivo was found to decrease from pup (40.7 mM) to adolescent (11.1 mM) to the mature/old groups (2.6/1.2 mM); however, a large difference in low-affinity site number was only observed between pup and adolescent bone extracts. The overall organic composition of EDTA and guanidine-HCl extracts generally reflected the composition of total bone, which dropped dramatically on a dry weight basis from pup to adolescent groups. A similar pattern was observed with the number of low-affinity binding sites measured in vitro. In vitro binding data indicate that nonmineralized matrix of pup bone, extractable by 4 M guanidine-HCl, possesses enough capacity to accommodate approximately 40% of the readily exchangeable pool. As age progresses, other components of the blood-bone exchange process, such as vascularity, may reduce the readily exchangeable calcium pool size below the amount of low-affinity sites measured in vitro.

Receptor and postreceptor insulin resistance induced by in vivo hyperinsuiinemia

1983 ◽  
Vol 61 (8) ◽  
pp. 802-807 ◽  
Author(s):  
C. Martin ◽  
K. S. Desai ◽  
G. Steiner
Keyword(s):  
Insulin Resistance ◽  
Glucose Oxidation ◽  
Binding Capacity ◽  
Insulin Receptors ◽  
Insulin Binding ◽  
Insulin Concentration ◽  
Fat Cell ◽  
And Control

We examined the effects of inducing hyperinsuiinemia in vivo in rats on the insulin receptors of, and the glucose oxidation by their adipocytes. Hyperinsulinemia was induced over a 2-week period by injecting NPH insulin subcutaneously. This was given in doses that were gradually increased to a final dose of 6 units/day. Profound hypoglycemia was avoided by providing supplemental sucrose to both the insulin-treated and control rats. The insulin concentration was eight times greater in the insulin-treated rats. However, they were not grossly obese and their adipocytes were not enlarged. The adipocytes of the hyperinsulinemic rats had a 25% lower maximal insulin binding capacity and were resistant to the effects of insulin on glucose oxidation. We felt that the hyperinsuiinemia was sufficient so that, despite their somewhat lower insulin binding capacity, these adipocytes would not bind less insulin in vivo than would adipocytes from control rats. Hence, we postulated that, this massive hyperinsulinemia not only down regulated the insulin receptor, but also led to a postreceptor resistance. This notion was supported by two lines of in vitro data. First, even at maximally effective medium concentrations of insulin, the maximum rate of glucose oxidation by the adipocytes from hyperinsulinemic rats reached a plateau which was less than that reached by cells from controls. Second, when this in vitro glucose oxidation was related not merely to the medium insulin concentration, but to the amount of insulin bound to adipocytes, the response of the hyperinsulinemic rats' cells was always lower than control. These changes occurred in the absence of any difference in fat cell size. Thus, in vivo hyperinsulinemia led to insulin resistance in adipocytes. This was associated both with down regulation of the insulin receptors and with a postreceptor defect.

Ultrastructural Correlations between Clonal Human Tumor Colonies and in Vivo Neoplasms

1982 ◽  
Vol 40 ◽  
pp. 210-211
Author(s):  
M.J. Murphy ◽  
R.R. Price ◽  
J.C. Sloman
Keyword(s):  
Cultured Cells ◽  
Human Tumor ◽  
Cell Type ◽  
Tumor Mass ◽  
Initial Cell ◽  
Cloning Assay ◽  
Human Tumor Cloning ◽  
The Relationship

The in vitro human tumor cloning assay originally described by Salmon and Hamburger has been applied recently to the investigation of differential anti-tumor drug sensitivities over a broad range of human neoplasms. A major problem in the acceptance of this technique has been the question of the relationship between the cultured cells and the original patient tumor, i.e., whether the colonies that develop derive from the neoplasm or from some other cell type within the initial cell population. A study of the ultrastructural morphology of the cultured cells vs. patient tumor has therefore been undertaken to resolve this question. Direct correlation was assured by division of a common tumor mass at surgical resection, one biopsy being fixed for TEM studies, the second being rapidly transported to the laboratory for culture.

In Vitro and in Vivo Comparison of Binding of 99m-Tc-Iabeled Anti-CEA MAb F33-104 with 99m-Tc-labeled Anti-CEA MAb BW431/26

1999 ◽  
Vol 38 (04) ◽  
pp. 115-119
Author(s):  
N. Oriuchi ◽  
S. Sugiyama ◽  
M. Kuroki ◽  
Y. Matsuoka ◽  
S. Tanada ◽  
...  
Keyword(s):  
Nude Mice ◽  
Binding Capacity ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
Cell Binding ◽  
Vitro Binding ◽  
Labeling Method ◽  
Human Colon Adenocarcinoma

Summary Aim: The purpose of this study was to assess the potential for radioimmunodetection (RAID) of murine anti-carcinoembryonic antigen (CEA) monoclonal antibody (MAb) F33-104 labeled with technetium-99m (99m-Tc) by a reduction-mediated labeling method. Methods: The binding capacity of 99m-Tc-labeled anti-CEA MAb F33-104 with CEA by means of in vitro procedures such as immunoradiometric assay and cell binding assay and the biodistribution of 99m-Tc-labeled anti-CEA MAb F33-104 in normal nude mice and nude mice bearing human colon adenocarcinoma LS180 tumor were investigated and compared with 99m-Tc-labeled anti-CEA MAb BW431/26. Results: The in vitro binding rate of 99m-Tc-labeled anti-CEA MAb F33-104 with CEA in solution and attached to the cell membrane was significantly higher than 99m-Tclabeled anti-CEA MAb BW431/261 (31.4 ± 0.95% vs. 11.9 ± 0.55% at 100 ng/mL of soluble CEA, 83.5 ± 2.84% vs. 54.0 ± 2.54% at 107 of LS 180 cells). In vivo, accumulation of 99m-Tc-labeled anti-CEA MAb F33-104 was higher at 18 h postinjection than 99m-Tc-labeled anti-CEA MAb BW431/26 (20.1 ± 3.50% ID/g vs. 14.4 ± 3.30% ID/g). 99m-Tcactivity in the kidneys of nude mice bearing tumor was higher at 18 h postinjection than at 3 h (12.8 ± 2.10% ID/g vs. 8.01 ± 2.40% ID/g of 99m-Tc-labeled anti-CEA MAb F33-104, 10.7 ± 1.70% ID/g vs. 8.10 ± 1.75% ID/g of 99m-Tc-labeled anti-CEA MAb BW431/26). Conclusion: 99m-Tc-labeled anti-CEA MAb F33-104 is a potential novel agent for RAID of recurrent colorectal cancer.

scholarly journals Stage-dependent effect of deferoxamine on growth of Plasmodium falciparum in vitro

Blood ◽  
1990 ◽  
Vol 76 (6) ◽  
pp. 1250-1255 ◽  
Author(s):  
S Whitehead ◽  
TE Peto
Keyword(s):  
Plasmodium Falciparum ◽  
Growth Inhibition ◽  
Antimalarial Activity ◽  
Clinical Malaria ◽  
Inhibitory Effect ◽  
Parasite Development ◽  
And Control ◽  
Speed Of Onset

Abstract Deferoxamine (DF) has antimalarial activity that can be demonstrated in vitro and in vivo. This study is designed to examine the speed of onset and stage dependency of growth inhibition by DF and to determine whether its antimalarial activity is cytostatic or cytocidal. Growth inhibition was assessed by suppression of hypoxanthine incorporation and differences in morphologic appearance between treated and control parasites. Using synchronized in vitro cultures of Plasmodium falciparum, growth inhibition by DF was detected within a single parasite cycle. Ring and nonpigmented trophozoite stages were sensitive to the inhibitory effect of DF but cytostatic antimalarial activity was suggested by evidence of parasite recovery in later cycles. However, profound growth inhibition, with no evidence of subsequent recovery, occurred when pigmented trophozoites and early schizonts were exposed to DF. At this stage in parasite development, the activity of DF was cytocidal and furthermore, the critical period of exposure may be as short as 6 hours. These observations suggest that iron chelators may have a role in the treatment of clinical malaria.

Preparation of dextran–casein phosphopeptide conjugates, evaluation of its calcium binding capacity and digestion in vitro

2021 ◽  
pp. 129332
Author(s):  
Lan Jiang ◽  
Shuhong Li ◽  
Nan Wang ◽  
Shuang Zhao ◽  
Yue Chen ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Binding Capacity ◽  
Casein Phosphopeptide

scholarly journals Role of interleukins in the pathogenesis of pulmonary fibrosis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yi Xin She ◽  
Qing Yang Yu ◽  
Xiao Xiao Tang
Keyword(s):  
Pulmonary Fibrosis ◽  
Therapeutic Strategy ◽  
Future Directions ◽  
Regulation Mechanisms ◽  
Underlying Mechanisms ◽  
Multiple Cells ◽  
The Relationship

AbstractInterleukins, a group of cytokines participating in inflammation and immune response, are proved to be involved in the formation and development of pulmonary fibrosis. In this article, we reviewed the relationship between interleukins and pulmonary fibrosis from the clinical, animal, as well as cellular levels, and discussed the underlying mechanisms in vivo and in vitro. Despite the effects of interleukin-targeted treatment on experimental pulmonary fibrosis, clinical applications are lacking and unsatisfactory. We conclude that intervening in one type of interleukins with similar functions in IPF may not be enough to stop the development of fibrosis as it involves a complex network of regulation mechanisms. Intervening interleukins combined with other existing therapy or targeting interleukins affecting multiple cells/with different functions at the same time may be one of the future directions. Furthermore, the intervention time is critical as some interleukins play different roles at different stages. Further elucidation on these aspects would provide new perspectives on both the pathogenesis mechanism, as well as the therapeutic strategy and drug development.

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