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Biomedical subjects

E Sander

Publications and source records attributed to E Sander.

At least 19 recordsLinked to original sources
PubMed1992

CD69, an early activation antigen on lymphocytes, is constitutively expressed by human epidermal Langerhans cells.

When screening skin cryosections with a panel of monoclonal antibodies (MoAb), we found that the anti-CD69 MoAb Leu-23 reacted with a subpopulation of epidermal dendritic cells, presumably Langerhans cells (LC). The staining intensity was enhanced by gentle trypsin pretreatment of the sections. Flow cytometric analysis of LC-enriched epidermal cells (EC) revealed that nearly all CD1a-bearing LC display anti-CD69 reactivity when tested briefly after termination of the enrichment procedure. Immunoprecipitation experiments showed that isolated LC specifically express a disulphide-linked dimer composed of 26/30kDa subunits that therefore slightly differs from the 28/32kDa CD69 complex described on activated T or natural killer (NK) cells. This difference is probably due to a different post-translational glycosylation pattern as evidenced by Endoglycosidase-F treatment of the immunoprecipitate disclosing the 24-kDa core protein of CD69. When freshly isolated LC-enriched EC were kept in culture, anti-CD69 reactivity gradually decreased but the addition of IFN-gamma to the culture medium sustained the CD69 expression on LC in vitro. These results strongly suggest that resident but not LC recovered from EC cultures bear CD69 moieties. It remains to be seen whether the expression of this antigen can be linked to (a) particular functional property (ies) of intraepidermal LC.

Antibodies, Monoclonal↗
PubMed1992

Osteochondroma in laboratory rats: a report of 3 cases in a Fischer-344, a Sprague-Dawley, and a Wistar rat.

Three cases of osteochondroma in a male Sprague-Dawley (SD) rat, a female Fischer (F344) rat, and a male Wistar rat are described. The rats were aged between 26 and 30 months. All osteochondromas were considered to be of spontaneous origin. The Wistar rat had multiple osteochondromas on both hind legs, the skull base, and a lumbar vertebra, whereas each of the F344 and SD rats was affected by a solitary osteochondroma, also on a lumbar vertebra. The lumbar osteochondromas were similar in appearance in all rats and consisted of a central core of trabecular bone, interspersed with fatty marrow and covered by a cap of hyaline cartilage. The additional tumors in the Wistar rat represented different developmental stages of osteochondroma with or without endochondral activity. The osteochondromas in the rats were morphologically similar to those described in humans and some domestic animal species.

Animals↗
PubMed1992

Monoclonal antibody to tumor necrosis factor--alpha prevents lethal endotoxin sepsis in adult rhesus monkeys.

In a rhesus monkey endotoxin sepsis model established by intravenous administration of 300 mg/kg D-galactosamine and 0.1 microgram/kg lipopolysaccharide from Salmonella abortus equi, hemodynamic, respiratory, metabolic and hematologic variables; levels of blood gases; monkey leukocyte elastase levels, and blood plasma concentrations of tumor necrosis factor--alpha (TNF) were monitored for 6 hours after administration, and again after 24 hours. Thirty minutes after administration of lipopolysaccharide, either 15 mg/kg anti-TNF monoclonal antibody (MoAB; n = 6) or vehicle placebo (saline solution; n = 4) were given intravenously. During this short-term experiment the organ functions were not different between the treatment groups. However, anti-TNF MoAb afforded morphologic protection from heart, lung, liver, and kidney damage after lipopolysaccharide challenge. Coagulation responses (platelet count and levels of fibrinogen, antithrombin III, and thrombin-antithrombin III complex) were smaller in anti-TNF MoAB-treated monkeys. Plasma TNF levels (WEHI cell cytotoxicity assay) reached a peak (350 pg/ml) 60 minutes after lipopolysaccharide administration in vehicle control subjects but no TNF was detected in the anti-TNF MoAB-treated monkeys. All control animals died 67 +/- 30 hours after lipopolysaccharide administration from multiorgan failure. On the contrary, all anti-TNF MoAB-treated animals survived 14 days (p > 0.005 vs placebo group mortality). Thus in short-term monkey experiments our study indicates protection against lipopolysaccharide-induced endotoxin sepsis by anti-TNF MoAB, which may have clinical relevance for the treatment of human septicemia.

Acid-Base Imbalance↗
PubMed1991

Phase II study of teniposide in patients with AIDS-related Kaposi's sarcoma.

Antitumour activity of cytotoxic agents, evaluated in patients with AIDS-related Kaposi's sarcoma (KS), is about 30-80%. However, responses are mostly partial and short. Experience with etoposide is similar. Teniposide has a longer elimination half-life and superior antitumour activity compared with etoposide in some experimental models. Thus a phase II trial was done in 25 patients with AIDS-related KS. Teniposide was given by 60-min infusion at 360 mg/m2 every 3 weeks. 10 (40%) showed a partial response, median duration of 9 (6-20) weeks. The main side-effects were leukopenia, thrombocytopenia, nausea and vomiting, alopecia and mucositis.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Effect of postural stimulation on systemic hemodynamics and sympathetic nervous activity in systemic hypertension.

The contributions of the carotid sinus and cardiopulmonary baroreflexes to the interindividual variation in sympathetic nervous system activation caused by postural adaptation were indirectly assessed in 68 mild hypertensive subjects. Supine and upright plasma norepinephrine (NE), blood pressure (cuff) and cardiac output (acetylene rebreathing) were measured. Mean arterial pressure (MAP), carotid sinus pressure, stroke volume and systemic vascular resistance were calculated. Stroke volume was assumed to be proportional to the degree of stretch of cardiac mechanoreceptors, carotid sinus MAP was assumed to be proportional to carotid sinus stretch and plasma NE to reflect sympathetic nervous activity. Plasma NE correlated inversely with stroke volume (r = -0.62, p less than 10(-14] and estimated carotid sinus MAP (r = -0.33, p less than 0.0002) and positively with systemic vascular resistance (r = 0.59, p less than 10(-10]. Holding systemic vascular resistance constant by partial regression, the inverse relation between plasma NE and stroke volume remained (partial r = -0.36, p less than 0.02). Multiple linear regression yielded the equation: plasma NE (pg/ml) = 720 + 4.3 age - 5.1 stroke volume (ml) - 1.0 carotid sinus MAP (mm Hg). Substituting mean supine and upright values for stroke volume and carotid sinus MAP in this equation, it can be roughly estimated that changes in stroke volume account for as much as 60% of the postural variation in plasma NE in hypertensives, whereas only 15% of this variation is caused by changes in carotid sinus pressure. These findings suggest that cardiopulmonary baroreflexes are primary activators of the sympathetic nervous system during postural adaptation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Hemodynamics of seasonal adaptation.

To investigate the possibility that seasonal adaptation requires significant hemodynamic changes, 5 normotensive and 21 mildly hypertensive subjects were followed through 4 seasons for changes in systemic hemodynamics and sympathetic nervous activity. In the upright position wintertime blood pressures increased by 3% (P = NS) over summer values whereas cardiac output and stroke volume decreased by 18% and 21%, respectively (P less than .0017 for each). Similarly, wintertime upright heart rate increased by 7% (P less than .017) with larger parallel increases in systemic vascular resistance (+24%, P less than .0017) and plasma norepinephrine (+26%, P less than .017). The supine values followed similar trends but the magnitude of changes was about 50% less than the corresponding upright values. Thus, in the northern US, wintertime vasoconstriction is related to increased sympathetic nervous activity and decreased cardiac output. When these reciprocal changes are proportional, blood pressure remains constant.

Adaptation, Physiological↗
PubMed1990

Characterization of Bay U 3405, a novel thromboxane A2/endoperoxide receptor antagonist.

The thromboxane A2-receptor antagonistic properties of Bay U 3405 [(3R)-3-(4-fluorophenylsulfonamido)-1,2,3,4-tetrahydro-9-carbaz o-lepropanoic acid] have been evaluated in various pharmacologic models. Bay U 3405 specifically inhibits platelet aggregation induced by U 46619, collagen, platelet-activating factor, and the second wave of ADP (IC50 0.5, 0.07, 0.3, 0.19 microM) in human plasma. The plasma phase of ADP-induced aggregation is not affected. U 46619-induced platelet aggregation is competitively antagonized (pA2 = 6.3). In humans, ex vivo platelet aggregation is inhibited after oral application of 2 or 50 mg Bay U 3405. Bay U 3405 also specifically and competitively antagonizes U 46619-induced contractions of rabbit aortic rings (pA2 = 7.4). In vivo, Bay U 3405 protects rabbits dose dependently from arachidonic acid or collagen-induced thromboembolism (ED50 1-3 mg/kg p.o). Chronic administration of Bay U 3405 to stroke-prone spontaneously hypertensive rats reduces stroke-related mortality and diminishes the occurrence of cerebral hemorrhages. From these results, we conclude that Bay U 3405 is an orally active, selective, and competitive thromboxane A2-receptor antagonist that may be beneficial in the treatment of cardiovascular or cerebrovascular diseases.

Adenosine Diphosphate↗
PubMed1989

[Fracture of the tibial shaft--still a traumatology problem?].

Diaphyseal fractures of the lower leg have continued to hold a special position in terms of incidence, type, severity, and frequency of typical complications as well as healing disorders. Despite general consensus regarding fracture healing and major factors of influence, there still is discrepancy of opinions and recommendations, in the context of pathophysiology, mechanics, and therapy. All in all, 302 fresh fractures and 134 cases of delayed healing or pseudoarthrosis in the diaphyseal region were treated, between 1971 and 1985. It has been the authors' experience that conservative treatment, according to the classical school, should be applied whenever possible. The trend in surgery, primarily for open fractures, is towards adequately dimensioned fixateur externe. Accurately defined minimum instability and healing with callus formation are nowadays appreciated and preferred. The fibula-ligament-membrane-complex may assume great importance to instable or defective forms of tibial fractures. Experimental and clinical investigations are likely to suggest that, depending on the individual case, the fibula should be included in the overall therapeutic concept, when it comes to impaired or delayed healing and pseudoarthrosis.

Adolescent↗
PubMed1982

Monoclonal antibodies against a plant virus.

Eight stable hybridoma clones derived from fusion of spleen cells of Tobacco Mosaic Virus (TMV) immunized mice with murine myeloma cells were grown in mass culture. They were obtained by 2 subsequent limiting dilution cloning cycles and subcultivation. Five of these clones secreted monoclonal antibodies which reacted with TMV nucleocapsid but not with capsid monomers and the monoclonal antibodies secreted by 3 other clones reacted with the TMV capsid monomer but not with the nucleocapsid. The specificity was determined by Enzyme Linked Immunosorbent Assay (ELISA) adjusted for the detection of antibodies in hybridoma culture supernatants.

Animals↗
PubMed1979

Basement membrane thickness, insulin antibodies and HLA-antigens in long standing insulin dependent diabetics with and without severe retinopathy.

The study was designed to show whether there was any relation between muscle capillary basement membrane thickness, HLA-antigens, anti-insulin antibodies and proliferative retinopathy. Electron microscopic measurements of muscle capillary basement membrane thickness were performed on muscle biopsies from 15 insulin-dependent diabetics and severe proliferative retinopathy, 24 insulin-dependent diabetics with minimal retinopathy and 18 age- and sex matched non-diabetics. All the patients had had diabetes for 20 years or more. None had biochemical or clinical evidence of diabetic nephropathy. Basement membrane thickness was measured according to the methods of Siperstein and Williamson. Muscle capillary basement membrane thickening occurred in 32 of 39 diabetics, using the Siperstein method, but patients with proliferative retinopathy did not exhibit thicker basement membranes than patients with no or minimal changes in the retina. There were apparent differences in HLA-antigens between diabetics with and without proliferative retinopathy, but they did not reach statistical significance. There was no correlation between muscle capillary basement membrane thickness and the quantity of insulin antibodies. The results indicate that factors other than basement membrane thickening and genetic factors in the HLA-region, are responsible for the development of proliferative retinopathy.

Adult↗