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Biomedical subjects

E Linder

Publications and source records attributed to E Linder.

At least 145 records · Page 8Linked to original sources

Autoantibodies against the inner aspect of erythrocyte membranes in NZB mice.

Erythrocyte autoantibodies in NZB mice react by hemagglutination methods with exposed and hidden red cell antigens. The hidden antigens can be exposed by treatment with proteolytic enzymes. By indirect immunofluorescence one antibody population can be shown to react with modified red cells. In the present study the location of the corresponding autoantigen within the membrane was studied. Mechanical or hypotonic lysis of the red cells exposed the antigen. Proteolytic digestion known to expose other erythrocyte autoantigens had no effect. The autoantigen was exposed on 'inside out' erythrocyte membrane vesicles, but not on 'right-side out' vesicles, prepared from isolated erythrocyte ghosts. Frezzing and thawing as well as mechanical disintergration of red cells liberated antigenically active material as saline-insuluble fibrillar material. The observations indicate that the autoantigen studied is located at the inner aspect of the erythrocyte membrane and suggest that it is associated with fibril-forming structural components. The observed reactivity distinguishes the described antibodies from previously identified erythrocyte autoantibodies.

Animals↗

Connective tissue origin of the amyloid-related protein SAA.

Protein SAA is a serum protein related to the major constituent of secondary amyloid fibrils, protein AA, and has been suggested to be a precursor of the amyloid protein AA. In the present study, the origin of SAA was investigated by studying human fetal tissues and cultured human fetal fibroblasts with the indirect immunofluorescence technique. Anti-SAA antibodies reacted strongly with cultured fibroblasts producing a fine fibrillary cytoplasmic staining and with extracellular fibrils in loose connective tissues and vessel walls. The reactions were specifically inhibited by absorption with degraded amyloid material, isolated protein AA, isolated protein SAA, and sera from patients with elevated levels of SAA. In contrast, no inhibition was seen with amyloid fibril material devoid of AA protein or by human sera in which SAA was not detectable by double-diffusion tests. These observations showed that SAA-like material is produced by fibroblasts and indicate that it is a normal constituent of developing extracellular connective tissue fibers.

Amyloid↗

Fibroblast surface antigen (SF): molecular properties, distribution in vitro and in vivo, and altered expression in transformed cells.

We have recently described a cell type-specific surface (SF) antigen that is deleted in chick fibroblasts transformed by Rous sarcoma virus, SF antigen is a major surface component and makes up about 0.5% of the total protein on normal cultured fibroblasts. The antigen is shed from normal cells and is present in circulation (serum, plasma), and in vivo, also, in tissue boundary membranes. The molecular equivalents of both cellular and serum SF antigen are distinct, large polypeptides, one of which (SF210, MW 210,000) is glycosylated and, on the cell surface, highly susceptible to proteases and accessible to surface iodination. Immunofluorescence and scanning electron microscopy have indicated that the antigen is located in fibrillar structures of the cell surface, membrane ridges, and processes. Human SF antigen is present in human fibroblasts and in human serum. We have recently shown that human SF antigen is identical to what has been known as the "cold-insoluble globulin" and that it shows affinity toward fibrin and fibrinogen. Our results also indicate that loss of the transformation-sensitive surface proteins is due not to loss of synthesis but to lack of insertion of the protein in the neoplastic cell surface. Both normal and transformed cells produce the SF antigen, but the latter do not retain it in the cell surface. The loss of SF antigen, a major cell surface component, from malignant cells creates an impressive difference between the surface properties of normal and malignant cells. The possible significance of SF antigen to the integrity of the normal membrane and its interaction to surrounding structures is discussed.

Animals↗

Prozone effects in indirect immunofluorescence.

A marked prozone effect was observed in indirect immunofluorescence (IFL) with rabbit antisera against rat renal proximal tubular epithelial brush border (BB) antigens: anti-BB antibodies were not detectable if used in high concentrations but were readily demonstrated if sufficiently diluted. The prozone effect occurred in spite of demonstrated binding of anti-BB antibodies to target antigens. No prozone was seen when direct IFL was used, and 'cross-reacting' antigens in small-intestinal epithelial brush border were detectable by indirect IFL without prozone. It was concluded that the anti-immunoglobulin conjugates were unable to reach antigenic determinants on tightly clustered immunoglobulin molecules. Thus prozone effects seem to depend primarily on the density of antigen determinants in the target tissues.

Animals↗

The haemodynamic effects of adrenergic receptor blockade or stimulation druing nitrous oxide anaesthesia in dogs.

The effects of ventilation with normoxic and hyperoxic nitrous oxide on systemic, pulmonary and coronary haemodynamics before and after adrenergic receptor blockade or stimulation were investigated in 15 dogs. To evaluate a blocking or stimulating effect of nitrous oxide on the alpha-adrenergic receptors, the animals were given phenoxybenzamine or noradrenaline, respectively. The effects of beta-adrenergic receptor blockade or stimulation were studied after injection of propranolol or isoproterenol, respectively. The experiments showed that in spite of the lack of alpha-receptor blocking properties and despite the tendency to produce beta-receptor blockade, nitrous oxide induced vasodilation. The findings of the present study, together with the increase in cardiac output and peripheral vasodilation, suggest that the cardiovascular effects of nitrous oxide are extra-adrenergic.

Anesthesia, Inhalation↗

The haemodynamic effects of nitrous oxide anaesthesia on myocardial blood flow in dogs.

The effects of ventilation with nitrous oxide in oxygen on myocardial blood flow any oxygen metabolism were investigated in 31 mongrel dogs. The results of this study showed that, compared with controls, hyperoxic nitrous oxide mixtures did not cause any great changes in myocardial haemodynamics, despite a decrease in cardiac output and an increase in systemic vascular resistance. Normoxic nitrous oxide mixtures produced an increase of the coronary blood flow due to decreased coronary vascular resistance. To what extent this coronary vasodilatation resulted from a increased myocardial metabolism or from a direct effect of nitrous oxide on the coronary vascular bed cannot be quantified from the present results.

Anesthesia, Inhalation↗

The haemodynamic effects of nitrous oxide anaesthesia on systemic and pulmonary circulation in dogs.

The haemodynamic effects of nitrous oxide in normoxia (20% oxygen) and in hyperoxia (50% oxygen) were investigated in 13 dogs. Nitrous oxide in hyperoxia caused a significant rise in total peripheral resistance and a significant decrease in cardiac output, heart rate, myocardial contractility (dP/dt max) and cardiac work. On the other hand, nitrous oxide in normoxia seemed to reverse these findings and did not exert negative inotropic effects on the myocardium. The results indicate that the earlier reported sympathetic activation of the circulation may be related to hyperoxia and not to nitrous oxide as such.

Anesthesia, Inhalation↗

[Silicone rubber-- an unsuitable and dangerous material for T-drains].

Four cases of bile peritonitis after removal of silastic T-tubes are described. The removal of the tubes took place 8 to 23 days after operation. This complication has been described only since the introduction of silastic tubing. The therapy consists in early relaparotomy and drainage. In dogs, the behavior of intraperitoneal silastic and rubber tubes was compared. Whereas rubber tubing was completely surrounded by a fibrous sheet not later than 2 weeks after implantation, the silastic tubing was floating freely in the abdominal cavity even after 6 weeks. Therefore, the use of silastic tubes is dangerous in short-time bile duct drainage. On the other hand, this material had advantages for long-term drainage and for endoluminal prostheses.

Adult↗

Membrane antigens shared by renal proximal tubules and other epithelia associated with absorption and excretion.

The distribution of shared antigens in specialized surface membranes of epithelia associated with absorption and excretion was studied using antisera against isolated epithelial brush borders of renal proximal tubules. Rabbits were immunized with a membrane fraction isolated from rat kidneys and the reactions of the resulting heterologous antisera with different rat organs were studied by immunofluorescence. The antisera reacted with the following structures: epithelial brush border of renal proximal tubules, bile canaliculi and bile duct epithelium of the liver, epithelial brush border of the intestinal villi, luminal parts of some epididymal tubules, allantochorionic epithelium, and apical parts of the exocrine epithelium of the pancreatic, salivary and lacrimal glands. Both quantitative and qualitative differences in antigen contents were suggested by absorption experiments.

Animals↗

Distribution of fibroblast surface antigen in the developing chick embryo.

Fibroblast surface (SE) antigen is present in fibrillar surface structures of cultured normal fibroblasts, shed to the extracellular medium, and is also found in circulation (serum and plasma). Malignant fibroblasts (transformed by viruses) do not express SF antigen on the cell surface. In this study the in vivo differentiation and distribution of SF antigen has been investigated in the developing chick embryo using cryostat sections and immunofluorescence. The major findings were: (a) SF antigen was detectable in the loose connective tissue of very early (2-to 3-day old) embryos. (b) Condensation of SF antigen was seen in various boundary membranes such as the glomerular and tubular basement membranes of the kidney, the boundary membranes of the notochord, yolk sac, and vitelline membranes and liver sinusoids. (c) SF antigen was found to be cell-type specific. It was seen as a fibrillar network in the loose connective tissue of different organs but not in the parenchymal cells. It was not found in muscle cells at any stage of development. (d) The antigen was present in the undifferentiated mesenchymal cells of the kidney; but not found after their development into epithelial cells of the secretory tubules. (e) Both in vivo and in fibroblast cultures SF antigen was distributed as a fibrillar network. These data indicate that SF antigen is a "differentiation antigen" restricted to certain cells of mesenchymal origin and character, and that is accumulates in the connective tissue during embryogenesis.

Animals↗

An inhibitor of chemotaxis and phagocytosis in reticulum cell sarcoma.

In a study of neutrophil functions in haematological disorders using in vitro techniques, a heat-stable inhibitor of chemotaxis and phagocytosis was demonstrated in the plasma and serum of a 64-year-old woman with reticulum cell sarcoma. In partial purification by chromatography, the inhibitor activity could not be separated from IgG. Clinically the patient did not exhibit abnormal susceptibility to infections.

Aged↗

Distribution of fibroblast surface antigen: association with fibrillar structures of normal cells and loss upon viral transformation.

The localization of a cell type-specific, soluble fibroblast surface antigen (SFA) was studied by immunofluorescence and by scanning electron microscopy of the same cells. The antigen had an uneven distribution forming streaks on chick embryo fibroblasts. It was localized to membrane processes and ridges, with a diameter of 50-200 nm. The processes extended from the periphery of the cells to the substratum or to other cells. Trypsin treatment completely removed detectable amounts of SFA. The antigen was detectable within 1 h after trypsin-treated cells were reseeded. The reappearance of SFA correlated with the restoration of membrane processes. Fibroblasts transformed by Rous sarcoma virus (RSV) showed loss of all or most SFA. When normal cells were transformed without subcultivation and trypsinization a fibrillar extracellular network of SFA remained under the transformed fibroblasts while the cells themselves were negative in immunofluorescence. When fibroblasts infected by RSV mutants were transferred to nonpermissive temperature for transformation new SFA was detected within 2 h. These data lead us to propose that loss of stabilizing and anchoring effect of SFA molecules in fibrillar cell surface structures may be critical in altered growth control and malignant transformation.

Animals↗