The Theory of Tracer Experiments with <sup>131</sup>I-Labelled Plasma Proteins

Matthews, C. M. E.

doi:10.1088/0031-9155/2/1/305

Cited by 831 publications

(334 citation statements)

References 15 publications

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“…This indicates that the protein in this compartment corresponds with the intravascular protein pool. Hence, analysis based on the model proposed b) Matthews (1957) appears justified and it may be infened that compartment 2 corresponds with the interstitial fluid pool of protein. The significant fall in the distribution volume of compartment 1, on a live weight ba.sis, which was observed duriug exposure of rt'si.stant sheep suggests that plasma volume may have been reduced during this period.…”

Section: Discussionmentioning

confidence: 99%

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IMMUNOGLOBULIN METABOLISM IN SHEEP INFECTED WITH THE SMALL INTESTINAL NEMATODE TRICHOSTRONGYLUS COLUBRIFORMIS

Steel

1978

Aust J Exp Biol Med

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Summary Radiotracer techniques were used to compare the kinetics of IgG1 and IgG2 metabolism in sheep (1) prior to parasite exposure, (2) during an initial patent infection with Trichostrongylus colubriformis, and (3) during continuous exposure to the parasite when the animals were exhibiting resistance. Plasma concentrations of IgG1, IgG2, IgA and IgM were also monitored throughout the experiment. Plasma IgG1 concentration increased significantly during the development of resistance and maintained this higher level on further exposure to the parasite. IgA concentration was also elevated during the development of resistance to a level approximately three times that observed prior to initial infection, hut this increase was only transitory. No significant changes in either IgG2 or IgM concentration occurred. Analysis of the radiotracer data for IgG1 and IgG2, was based on a two‐compartment model comprising intravascular and extravaseular protein pools with reversible exchange between them and irreversible loss from the intravascular site. No significant changes in compartment sizes or rates of exchange between compartments were recorded during measurement periods (1), (2) and (3) for either IgG1 or IgG2. Rates of irreversible loss of IgG2 were similar during (1), (2) and (3); the irreversible loss of IgG1 was unaltered following the initial infection but Increased by approximately 50% during period (3). It is concluded that increased synthesis of IgG1 in resistant sheep continually exposed to T. colubriformis occurs as a result of antigenic stimulation rather than as a consequence of increased loss of plasma into the intestine.

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Section: Discussionmentioning

confidence: 99%

“…DifFerences were considered significant at p < 0-05. Matthews, 1957). Compartnu-nt i represfnt.s tin-sampled intravascular compartniciit and compartment 2 the extravascular compartinent.…”

Section: Statistieal Analysismentioning

confidence: 99%

IMMUNOGLOBULIN METABOLISM IN SHEEP INFECTED WITH THE SMALL INTESTINAL NEMATODE TRICHOSTRONGYLUS COLUBRIFORMIS

Steel

1978

Aust J Exp Biol Med

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“…Plasma radioactivity curves were analyzed by the Matthews' method to calculate the fractional catabolic rate (FCR) , half-life (Ty2) and extravascular/intravascular ratios of the protein (20).…”

Section: Methodsmentioning

confidence: 99%

Metabolism of the third component of complement (C3) in patients with rheumatoid arthritis

Weinstein

Peters

Brown

et al. 1972

Arthritis & Rheumatism

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The metabolism of radioiodinated purified C3 was studied in 8 patients with classical seropositive rheumatoid arthritis, 1 patient with osteoarthritis, and 1 normal subject. An increased fractional catabolic rate and a decreased half-life was found in 2 subjects. Both these patients showed evidence of rheumatoid necrotizing vasculitis, and these results suggest an immune-mediated pathogenesis for this lesion. The high serum level of C3 found in some rheumatoid patients is due to an increased rate of C3 synthesis.Although the etiology of rheumatoid arthritis (KA) is obscure, there is much evidence implicating immune mechanisms in the pathogenesis of rheumatoid synovitis (1). Despite normal or elevated levels of hemolytic complement in the serum of rheumatoid patients (Z), low levels have been found consistently in rheumatoid synovial fluids (3), and more recently, synovial fluid degradation products of the third component of complement (C3) have been

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“…at time 0). The FCR was calculated by plasma curve analysis in all subjects [21] and by the metabolic clearance method of Berson & Yallow [22] in subjects with normal glomerular filtration rate (i.e. GFR 1 .…”

Section: Analysis Of Metabolic Datamentioning

confidence: 99%

The metabolism of C9 in normal subjects and in patients with autoimmune disease

Greenstein

Peake

Charlesworth

1996

Clinical and Experimental Immunology

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SUMMARYThe metabolism of the ninth component of complement (C9) was studied in eight healthy subjects and nine patients with autoimmune disease, including seven with systemic lupus erythematosus (SLE) and one each with mesangial IgA nephropathy and mixed essential cryoglobulinaemia. In normal subjects the metabolic parameters (mean Patients with reduced total serum haemolytic activity (i.e. CH 50 < 68% of normal human serum (NHS), n = 7) had significantly higher FCR (3 . 57 6 0 . 67%/h) and shorter T 1/2 (33 . 5 6 6 . 8 h) than the control group (both P < 0 . 05). The plasma concentration of the terminal complement complex (i.e. soluble TCC or SC5b-9) was higher in patients (median (range): 515 (300-1879 ¹ g/l)) than in normal subjects (313 (229-402 ¹ g/l); P < 0 . 01) and showed a positive correlation with the FCR of C9 (r = 0 . 61, P < 0 . 01). Plasma C9 production rate was also greater in patients (0 . 11 6 0 . 05 mg/kg per h) compared with control subjects (0 . 07 6 0 . 03 mg/kg per h, P < 0 . 05), and was associated with a higher C9 concentration in patients' sera (76 6 13 mg/l versus 61 6 14 mg/l, P < 0 . 05). These results demonstrate that C9 is rapidly metabolized in normal humans and that hypercatabolism occurs in patients with autoimmune disease and complement activation. This was despite the presence of normal or elevated serum C9 levels and normal compartmental distribution.

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The Theory of Tracer Experiments with ¹³¹I-Labelled Plasma Proteins

Cited by 831 publications

References 15 publications

IMMUNOGLOBULIN METABOLISM IN SHEEP INFECTED WITH THE SMALL INTESTINAL NEMATODE TRICHOSTRONGYLUS COLUBRIFORMIS

IMMUNOGLOBULIN METABOLISM IN SHEEP INFECTED WITH THE SMALL INTESTINAL NEMATODE TRICHOSTRONGYLUS COLUBRIFORMIS

Metabolism of the third component of complement (C3) in patients with rheumatoid arthritis

The metabolism of C9 in normal subjects and in patients with autoimmune disease

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The Theory of Tracer Experiments with 131I-Labelled Plasma Proteins

Cited by 831 publications

References 15 publications

IMMUNOGLOBULIN METABOLISM IN SHEEP INFECTED WITH THE SMALL INTESTINAL NEMATODE TRICHOSTRONGYLUS COLUBRIFORMIS

IMMUNOGLOBULIN METABOLISM IN SHEEP INFECTED WITH THE SMALL INTESTINAL NEMATODE TRICHOSTRONGYLUS COLUBRIFORMIS

Metabolism of the third component of complement (C3) in patients with rheumatoid arthritis

The metabolism of C9 in normal subjects and in patients with autoimmune disease

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Product

Resources

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The Theory of Tracer Experiments with ¹³¹I-Labelled Plasma Proteins