Search results for " pig"

An inherited deficiency of the third component of complement, C3, in guinea pigs

1986

Hereditary deficiency of the third component of complement, C3, is found very seldom in the human. C3 deficiency is associated with severe bacterial infections revealing the central role of C3 in complement activation via the classical or alternative pathway. We describe a new hereditary C3 deficiency in strain 2 guinea pigs. Serum from these animals had a markedly reduced lytic activity in a standard assay for complement-dependent, antibody-mediated cytotoxicity. In functional assays of individual components, the hemolytic activity of the components C4, C2, C5 and of factors B, D and H was in the normal range. The functional C3 titer, and similarly C3 antigenic activity in the serum of the…

Demonstration of High-Affinity Binding Sites for C3a Anaphylatoxin on Guinea-Pig Platelets

1978

3H-serotonin release from guinea-pig platelets was demonstrated to be the consequence of C3a binding to these cells. A Scatchard analysis of dose-response data of the 125I-C3a binding pattern to guinea-pig platelets pointed to the existence of binding sites with high and low affinity for the C3a molecule (HA and LA receptors). HA receptors are specific for C3a with intact C-terminal arginine. whereas C3adesarg only interacts with LA receptors. The release of serotonin may be induced by a combined reaction of C3a with HA receptors and LA receptors on the platelet membrane.

Comparative study on biological activities of various anaphylatoxins (C4a, C3a, C5a)

1981

Several anaphylatoxic substances (human C3a, guinea pig C3a, human C4a, guinea pig C5a, and a synthetic C3a-related hexapeptide) were compared with regard to their ability to induce secretion of [3H] serotonin from guinea pig platelets. Functional identity of the C3a preparations, C4a, and the hexapeptide was demonstrated by the phenomenon of crossed desensitization. Whereas C3a of human and guinea pig origin proved to be qualitatively and quantitatively identical, C4a expressed only 3% of the activity of the C3 fragments on a molar basis. Investigations with goat anti-guinea pig C3a demonstrate that human and guinea pig C3a possess one antigenic determinant in common; however, this determi…

Platelet Activation: a New Biological Activity of Guinea-pig C3a Anaphylatoxin

1978

3H-serotonin-release from labelled gp-platelets is established as a sensitive method for testing a new biological activity of gp-C3a anaphylatoxin in an autologous situation. Time-, dose- and temperature-dependent release reactions as well as specific inhibition by carboxypeptidase B and anti-C3a antibodies show that C3a is a potent and specific inducer of platelet activation. Inactive C3a does not induce 3H-serotonin-release but specifically inhibits the action of C3a on platelets.

Comparative study on biological effects of the guinea pig complement-peptide C3a and C3a-related synthetic oligopeptides

1980

Dose-response experiments with guinea pig C3a and a synthetic hexapeptide (amino acid residues 72–77), representing the COOH-terminal sequence of human C3a, were performed in two recently described bioassay systems for C3a, i.e. cytotoxicity against tumor cells measured as LDH and 51Cr-release and non cytolytic serotonin release from guinea pig platelets. Compared to the classical anaphylatoxic assay (guinea pig ileum contraction), nearly identical reactivities were observed in all three test systems with C3a and, although quantitatively different, with hexapeptide.

Characterization of the Purified Fourth Component of Guinea Pig Complement* *Supported by Deutsche Forschungsgemeinschaft (grant Kl 124/9).

1970

Publisher Summary A strain of rabbits deficient in complement was discovered in Freiburg, Germany in 1961. A second, clearly unrelated, strain was reported in Mexico. Both these strains are deficient in C6. A further complement-deficient rabbit was found by chance in Cambridge. This paper presents some data on the colony bred from this animal. C6 was partially purified from rabbit serum by chromatography on DEAE Cellulose and hydroxyapatite. Antibody to rabbit C6 in deficient rabbits was raised by four weekly injections of alum precipitated C6 with Bordetella pertussis as adjuvant into the knee joints, followed by three intravenous injections of the alum precipitated material without B. per…

Decreasing dietary linoleic acid promotes long chain omega-3 fatty acid incorporation into rat retina and modifies gene expression

2011

International audience; Age-related macular degeneration (AMD) may be partially prevented by dietary habits privileging the consumption of ω3 long chain polyunsaturated fatty acids (ω3s) while lowering linoleic acid (LA) intake. The present study aimed to document whether following these epidemiological guidelines would enrich the neurosensory retina and RPE with ω3s and modulate gene expression in the neurosensory retina. Rat progenitors and pups were fed with diets containing low or high LA, and low or high ω3s. After scotopic single flash and 8-Hz-Flicker electroretinography, rat pups were euthanized at adulthood. The fatty acid profile of the neurosensory retina, RPE, liver, adipose tis…

Dal colore alla caratterizzazione ottica di pigmenti antichi: validità del metodo spettrofotometrico e Teoria di Itten

2014

Functional foods and nutraceuticals: a way to improve health, prevent disease, and delay aging. The case of cactus pear.

2007

Cactus pear fruits have recently been the object of scientific research aimed at revealing bioactive components. This short review summarizes results obtained by our group. The two characteristic betalain pigments, betanin and indicaxanthin, appear promising molecules to be considered nutraceutical compounds.

The Role of Cadherins in Ca2+-Mediated Cell Adhesion and Inherited Photoreceptor Degeneration

2002

Cadherins are Ca2+-binding, transmembrane proteins involved in cell adhesion. Recently, three cadherin molecules, cadherin-23, protocadherin-15, and cadherin-3, were found to be defective in various human diseases, many of them with photoreceptor degeneration and/or sensorineural hearing loss as major features such Usher syndrome type 1D (USH1D), USH1F, and hypotrichosis with juvenile macular dystrophy. The process, by which mutations lead to photoreceptor degeneration is still not fully understood. Data from the inner ear phenotype of USH1 mouse models suggest that loss of cell adhesion is a crucial event.