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Biomedical subjects

E Muller

Publications and source records attributed to E Muller.

At least 19 recordsLinked to original sources
PubMed1995

The pathogenic role of Staphylococcus epidermidis capsular polysaccharide/adhesin in a low-inoculum rabbit model of prosthetic valve endocarditis.

BACKGROUND: The capsular polysaccharide/adhesin (PS/A) antigen of Staphylococcus epidermidis was required to produce endocarditis in a rabbit model in which infection resulted from hematogenous spread of bacteria from a contaminated catheter in the jugular vein. However, many prosthetic valve endocarditis (PVE) infections probably result from direct contamination of the valve with small numbers of bacteria during surgery. The role of PS/A in this situation was evaluated by modifying a rabbit model of endocarditis to partially mimic PVE. METHODS AND RESULTS: A Teflon catheter was contaminated with graded inocula of either PS/A-positive S epidermidis strain M187sp11 or the PS/A-negative, isogenic strain M187sn3 and inserted into the left ventricle through the aortic valve. The PS/A-positive strain had a 50% infectious dose of 1.1 x 10(2) cfu (95% CI, 3.3 to 3.7 x 10(3)) compared with 8.5 x 10(4) cfu of the PS/A-negative strain (95% CI, 8.6 x 10(3) to 8.5 x 10(5)). The odds for developing endocarditis were estimated to be 42 times higher for any given inoculum level of the PS/A-positive strain (P = .1). When the PS/A-positive strain was adherent to a catheter surface it survived in rabbit blood, whereas under the same conditions the PS/A-negative strain was killed approximately 90% in 1 hour. CONCLUSIONS: Direct contamination of an intraventricular foreign body by low levels of PS/A-positive S epidermidis results in endocarditis in rabbits, but at suitably high doses PS/A-negative strains have sufficient virulence to infect cardiac vegetations. PS/A enhances but is not absolutely required for bacterial virulence in a rabbit model of PVE.

Animals↗
PubMed1991

Oestrogen facilitates the binding of ubiquitous and liver-enriched nuclear proteins to the apoVLDL II promoter in vivo.

Using genomic and in vitro DNasel footprinting, we have analyzed protein-DNA interactions within the promoter region of the oestrogen-inducible gene encoding chicken apoVLDL II. The footprints coincide with previously detected guanosine-protein contacts in vivo. All footprints identified are present in the apoVLDL II-expressing liver exclusively and absent in hormone-naive liver, spleen and oviduct. They comprise recognition sites for the oestrogen receptor, the ubiquitous COUP-transcription factor, the liver-enriched C/EBP and/or DBP and the liver-specific LF-A1. In vitro, binding of protein to the oestrogen response element (ERE) is excluded by the prior binding of a protein, possibly C/EBP or DBP, to an adjacent element. The recognition sequence of the COUP-TF is also a target for LF-A1. The results suggests that oestrogen-dependent liver specific activation of the apoVLDL II promoter is established by the binding of the oestrogen receptor to EREs and multiple liver-enriched factors (C/EBP, DBP and LF-A1) to their nearby recognition sequences. Apparently, several DNA binding nuclear proteins cooperate to keep the promoter in a state that is accessible for the RNA polymerase complex.

Animals↗
PubMed1991

Blood proteins do not promote adherence of coagulase-negative staphylococci to biomaterials.

We studied the effects of in vitro and in vivo coating of catheters with human blood proteins on binding of coagulase-negative staphylococci. Coating resulted in no enhancement of binding. Catheters coated in vitro bound fewer organisms than uncoated catheters. Host proteins do not enhance adherence of coagulase-negative staphylococci to biomaterials.

Bacterial Adhesion↗
PubMed1991

Protection against endocarditis due to Staphylococcus epidermidis by immunization with capsular polysaccharide/adhesin.

BACKGROUND: Staphylococcus epidermidis is the principal pathogen in prosthetic valve endocarditis. The capsular polysaccharide adhesin (PS/A) has been shown to mediate attachment of bacteria to medical devices. In this study, we investigated the efficacy of active and passive immunization against PS/A in preventing S. epidermidis endocarditis in a rabbit model. METHODS AND RESULTS: Aortic valve vegetations were produced by inserting a Teflon catheter into the left ventricle through the right carotid artery. Bacteremia and endocarditis were then established by implanting in the left jugular vein a catheter that was attached to an osmotic pump and contaminated with S. epidermidis strain RP62A. During a 3-week study period, of 64 blood cultures taken every second or third day from six nonimmune rabbits, 54 (84%) yielded strain RP62A. In rabbits actively immunized with PS/A, eight of 60 blood cultures (13%) were positive (odds ratio 5.0, 95% CI, 2.0-12.3, p = 0.005). At death, all six nonimmune rabbits had infected vegetations that yielded 10(6)-10(11) colony-forming units (cfu)/g of vegetation, whereas only one PS/A-immunized rabbit had an infected vegetation. Immunization protocols designed to elicit antibody to teichoic acid but not to PS/A afforded no protection against bacteremia or endocarditis. Infusion of monoclonal antibody to PS/A through a catheter in the right jugular vein provided a level of protection against both bacteremia and endocarditis comparable to that produced by active immunization. In vitro, antibody against PS/A was opsonic for S. epidermidis. CONCLUSIONS: Immunoprophylaxis targeted at staphylococcal PS/A is a promising new approach to the prevention of prosthetic valve endocarditis.

Animals↗
PubMed1989

Lymphohaemopoietic antigens of cultured human glomerular epithelial cells.

Glomerular visceral epithelial cells (GVEC) from normal human glomeruli were grown in tissue culture. Cell surface markers were studied by immunofluorescence microscopy using antibodies against lymphohaemopoietic differentiation antigens which are known to be present early (BA-1, OKB2, BA-2) and late (J5, anti CR1) in renal ontogenesis. Like foetal human glomerular epithelium, the cultured cells reacted with BA-1 and OKB2 (identifying an antigen expressed on B cells and polymorphonuclear leucocytes), and BA-2 (leukaemia-associated antigen), but were consistently negative for CR1 (C3b receptor); J5 which identifies the common acute lymphoblastic leukaemia antigen (CALLA) stained variably. Reactivity with antimyosin or anti factor VIII were absent. The cells produced an extracellular matrix containing laminin, type IV collagen, and fibronectin. This study supports the notion that GVEC undergo dedifferentiation as shown by the acquisition of lymphohaemopoietic differentiation antigens present early in renal ontogeny. In addition, the production of extracellular matrix constituents in vitro may be useful for the investigation of human glomerular basement membranes.

Antibodies, Monoclonal↗
PubMed1988

T-cell modulation of the murine antibody response to Neisseria meningitidis group A capsular polysaccharide.

T-cell modulation of the antibody response of BALB/c mice to group A meningococcal capsular polysaccharide (PS) was examined by using an enzyme-linked immunosorbent assay. An optimal dose (5 micrograms) of antigen induced an immunoglobulin M (IgM) response of short duration; no IgG or IgA antibody could be detected. The capacity to produce serum antibody begins at about 3 weeks of age. Concanavalin A (ConA) inhibited the magnitude of the response by 40 to 60% when given at the time of immunization; it enhanced the response two- to eightfold when given 2 days after PS. T-cell-mediated suppression could be transferred to naive mice by injection of spleen cells from low-dose-primed mice. A secondary antibody response could be induced by immunization with live meningococci. Here, the IgM response was 8- to 10-fold greater than that of mice given an optimal dose of PS; IgG antibody against group A PS increased 1 week after immunization to levels that were 100- to 1,000-fold greater than those of mice immunized with PS. The antibody response could not be augmented by multiple injections of PS; suppression occurred after low-dose priming or hyperimmunization with PS. These studies indicate that the antibody response to PS is not completely T-cell independent; rather, it is inhibited and amplified by T cells.

Aging↗
PubMed1987

Functional identification of the perioral neuromuscular system: a signal flow diagram.

The components of a neuromuscular system are identified, and anatomical and physiological features of the elements are organized into a signal flow diagram. The elements of the perioral neuromuscular system are described in the context of the system flow diagram developed for a generalized neuromuscular system. Important features of commonality and contrast between limb and perioral systems, and areas of needed research are emphasized. Features of contrast include geometry and insertions of muscles, relative influence of inertial loads, and organization of inputs to motoneurons.

Facial Muscles↗
PubMed1986

Eye-derived growth factor isolated from bovine retina and used for epidermal wound healing in vivo.

Eye-derived growth factor (EDGF) has been found in several ocular tissues and shown to be able to stimulate the in vitro proliferation of cells from various tissues and organisms. It had already been shown that EDGF differs biochemically and biologically from other growth factors such as epidermal growth factor (EGF) and fibroblast growth factor in that it is the only one that can stimulate the in vitro growth of human adult keratinocytes. Moreover EDGF stimulates reepithelialization and neovascularization. In this paper we report data concerning the effect on the rate of epidermal wound healing in guinea pigs of different extracts obtained from adult bovine retina. Our results show that EDGF can significantly increase the rate of reepithelialization when epidermis is detached from dermis and removed after induction of a blister. The doses used were comparable to the ones used to obtain maximal increase of cell proliferation in vitro. However no attempt was made to further investigate the mechanism accounting for the observed wound healing. At 24 h, control wounds maintained under occlusive dressing had only about 50% of their surface covered with cells as opposed to EDGF-treated wounds which were covered up to about 80% (p = 0.05). On the other hand, EGF does not increase the rate of wound healing in this model even at 1000-fold higher doses than those used in in vitro bioassays. Although EDGF is still not purified to homogeneity and another 10- to 100-fold purification might be necessary to achieve homogeneity, our results suggest that EDGF may find therapeutic applications as a potent in vivo epidermal wound healing agent.

Animals↗
PubMed1984

Daily fluctuations in the activity of the tuberoinfundibular GABAergic system and plasma prolactin levels.

In view of the role exerted by gamma-aminobutyric acid (GABA) in the control of prolactin (PRL) secretion the circadian periodicity of hypothalamo-pituitary GABAergic activity and PRL secretion was evaluated in adult male rats to ascertain if a meaningful correlation between biochemical and endocrine indices may be evidenced. Anterior pituitary and median eminence GABA concentrations peaked during the late afternoon hours (18.00 h), while the glutamic acid decarboxylase activity reached higher concentrations at 15.00 h. Plasma PRL presented two circadian surges at 15.00 h and at midnight. Although the changes of GABA in the hypothalamo-pituitary complex and the PRL surges did not show a close temporal relation, the possibility may be considered that GABA circadian changes occurred as a delayed response to PRL circadian surges. However, it cannot be excluded that changes in the biochemical indices could be related to other neuroendocrine events.

Animals↗
PubMed1982

ACTH1-24 counteracts the prolactin-releasing effect of an opioid.

The administration of the synthetic and stable opioid peptide[D-Ala2,MePhe4,Met(O)5o1]enkephalin (FK 33-824) at the dose of 0.2 mg/kg i.v. induced a rise in plasma levels of prolactin in the rat, an effect which was prevented by 1 mg/kg i.v. of the opiate antagonist naloxone. A simultaneous i.v. injection of 20 microgram/kg i.v. of ACTH1-24 significantly reduced the prolactin releasing effect of FK 33-824, therefore giving further evidence of an in vivo interaction between ACTH-related peptides and opioid peptides.

Adrenocorticotropic Hormone↗
PubMed1981

Prolactin and the small intestine. Effect of hyperprolactinaemia on mucosal structure in the rat.

To study the mechanism for the adaptive mucosal hyperplasia which occurs independent of luminal nutrition and pancreatico-biliary secretions in isolated Thiry-Vella segments of intestine from lactating rats, and to examine the effects of prolactin on small bowel mucosal structure in the rat, we used two models of experimental hyperprolactinaemia and compared quantitative histology and several markers of mucosal mass in jejunum and ileum from control rats and from test and lactating animals. Hyperprolactinaemia, induced by perphenazine injections (5 mg/kg/day for two or seven weeks) or transplantation of four pituitary glands from donor animals to beneath the renal capsule in the recipient, was confirmed by radioimmunoassay. Proof of its biological activity was obtained by weighing the mammary pads and by demonstrating true breast hyperplasia on histological section. Median serum prolactin levels increased from 50 ng/ml in the controls to 570 ng/ml in the perphenazine treated animals and to 600 ng/ml in the pituitary transplanted rats-levels comparable with those seen in lactation (870 ng/ml). In the lactating rats, there was striking mucosal hyperplasia of both jejunum and ileum but, despite the hyperprolactinaemia, there were no such changes in villus height, crypt depth, or in mucosal wet weight, protein, or DNA/unit length intestine in the perphenazine-injected or pituitary-transplanted animals. We conclude that prolactin is not atrophic to the intestine in rats and that hyperprolactinaemia cannot explain the intestinal adaptive changes of lactation.

Animals↗
PubMed1977

relA gene control of the synthesis of lipid A fatty acyl moieties.

The incorporation of [14C]acetate into the fatty acid moieties of lipid A was measured during amino acid starvation of rel+ and relA strains of Escherichia coli K-12. The synthesis of the beta-hydroxymyristate and other fatty acid moieties was inhibited two- to fourfold in rel+ strains, whereas no inhibition was observed in relA strains. The fatty acid compositions of the phospholipids synthesized after amino acid starvation or rel+ and relA strains were also determined.

Acetates↗