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Biomedical subjects

M Körber

Publications and source records attributed to M Körber.

9 recordsLinked to original sources
PubMed2006

Stability of poly(D,L-lactide-co-glycolide) and leuprolide acetate in in-situ forming drug delivery systems.

In-situ forming drug delivery systems are prepared by dissolving a drug and a biodegradable polymer (poly(D,L-lactide-co-glycolide), PLGA) in a biocompatible organic solvent (In-situ implant, ISI) or further emulsified into an external phase (oil or aqueous solution), resulting in oil-in-oil or oil-in-water emulsions (In-situ forming microparticles, ISM). The chemical stability of PLGA and the drug is a major concern. In this study, the stability of PLGA and leuprolide acetate in the in-situ forming systems and lyophilized sponges was investigated. The degradation of PLGA increased with increasing storage temperature and water content in the biocompatible solvents. A faster degradation occurred in polar protic solvents (2-pyrrolidone, PEG 400, triethyl citrate) than in polar aprotic solvents (N-methyl-2-pyrrolidone, DMSO, triacetin, ethyl acetate). The presence of leuprolide acetate significantly accelerated PLGA degradation, especially in solution state. PLGA was stable in oily suspensions at 4 degrees C and degraded only slightly faster than solid powder at 25 degrees C. No interaction between the oils and the PLGA was observed as indicated by an unchanged T(g) of approx. 47 degrees C. PLGA underwent a slight degradation at 4 degrees C after 150 days in water and saturated sodium chloride solution. The degradation was slower in saturated sodium chloride solution than in water at 25 degrees C. Residual acetic acid in lyophilized sponges facilitated the PLGA degradation in contrast to dioxane. Leuprolide acetate did not affect the PLGA stability negatively. However, lidocaine significantly enhanced the polymer degradation in the sponges. Finally, leuprolide acetate was chemically stable in the sponges, the oils and the polymer solutions in suspension state, but unstable (aggregation) when dissolved in the polymer solutions and stored at 25 degrees C and 40 degrees C.

Chromatography, Gel↗
PubMed1998

Cardiac troponin I plasma levels for diagnosis and quantitation of perioperative myocardial damage in patients undergoing coronary artery bypass surgery.

OBJECTIVE: The definition of a reliable and generally accepted diagnostic standard for perioperative myocardial damage is desirable. Cardiac troponin I (cTnI) is highly specific for myocardial tissue and can be measured rapidly. The aim of our study was to evaluate the diagnostic potential of cTnI for myocardial lesions in patients undergoing coronary artery bypass surgery (CABG). METHODS: A total of 119 patients with diffuse coronary artery disease were operated on using blood cardioplegia. Serial blood samples drawn before and after surgery were analyzed for the activity of creatine kinase MB isoenzyme (CKMB) and the concentrations of CKMB mass, cardiac troponins T and I. On the basis of the biochemical results (except cTnI) and the findings of electrocardiography/echocardiography, patients were classified and cTnI was studied for each group separately: group I, minor myocardial damage; group II, non-transmural infarction; group III, transmural infarction; and group IV, preoperative non-transmural infarction. RESULTS: In 87 patients of group I (73.1%) cTnI levels remained low; 19 patients (16.0%) were assigned to group II, 8 patients (6.7%) to group III, and 5 patients (4.2%) to group IV. For discrimination of patients without and with perioperative myocardial infarction (PMI) by one cTnI determination, the use of cutoff values of 6.5 ng/ml at 8 h, 9.8 ng/ml at 12 h, and 11.6 ng/ml at 24 h after aortic unclamping resulted in a diagnostic efficiency of 88, 94 and 98%). Especially, a cTnI value at 24 h had a sensitivity of 100% and a specificity of 97%. Cardiac troponin levels at 24 h were found to correlate closely with the well-recognized 2-48 h area-under-the-curve (P < 0.0001; R = 0.993), making serial determinations unnecessary. CONCLUSIONS: cTnI qualifies as a marker for diagnosis of PMI and quantitation of the amount of myocardial damage, because of the availability of a quick diagnostic test with high specificity, the high diagnostic efficiency, and especially the sufficient information gained by a single determination 24 h after aortic unclamping.

Aged↗
PubMed1995

[Pentoxifylline inhibits secretion of O2- and TNF-alpha by alveolar macrophages in patients with sarcoidosis].

Reactive oxygen species (ROS) and cytokines like tumor necrosis factor-alpha (TNF-alpha) play a crucial role as inflammatory mediators in pulmonary sarcoidosis. We examined the antiinflammatory effect of pentoxifylline (POF) on alveolar macrophages (AM) of patients with sarcoidosis in vitro. We could demonstrate that POF (above 4.10(-4) M) inhibited the secretion of superoxide anion and TNF-alpha by AM in a dose-dependent manner via a prostaglandin synthesis-dependent mechanism that was independent of the glucocorticoid receptor. POF is an interesting immunomodulating substance that should be further evaluated in clinical trials.

Adult↗
PubMed1994

Oxidative metabolism of pulmonary phagocytes in acute pneumonia.

The oxidative response of activated phagocytes is a primary host defense mechanism in pneumonia, but is in addition capable of causing tissue damage. We evaluated amount and significance of the local oxidant production in immunocompetent and immunocompromised pneumonia patients; the relative contribution of neutrophils and alveolar macrophages to the total oxidant load was differentiated using chemiluminescence (CL) with different amplifiers. Luminol-enhanced CL correlated to neutrophil percentage and myeloperoxidase levels in the bronchoalveolar lavage and was markedly increased in both pneumonia groups. Lucigenin-enhanced CL was produced by both phagocyte types and not significantly increased. In both pneumonia groups elevated levels of serum proteins indicated severe alveolocapillary leakage. In conclusion the oxidative response in acute pneumonia was mainly due to neutrophil recruitment and activation; this defense mechanism was preserved even in severely immunocompromised patients.

Acute Disease↗
PubMed1991

[Vascular architecture of the skin in the postmortem microangiogram].

To demonstrate the detailed vascular architecture of the skin, barium sulphate suspension was injected into the arteries of nine amputated lower limbs. Sections of skin from the foot were fixed in formalin and embedded in paraffin and then examined by high resolution radiography. Subsequently histological sections were prepared and correlated with the micro-angiographic appearances. This technique provided demonstration of the detailed vascular structure of the skin with very little super imposition. The capillary loops in the papillae, the sub-papillary plexus, the glandular components (with the capillaries surrounding the sweat glands), the fine arteries and smallest veins in the cutis could be demonstrated over a prolonged course. Microangiographic and histologic sections were carried out in parallel. These eliminated artifacts and clarified the micro-angiographic appearances. The value of microangiography for demonstrating the vascularity of the skin under normal, pathological and experimental conditions is the subject of further studies.

Aged↗
PubMed1990

Significance of postoperative stability for bony reparation of comminuted fractures. An experimental study.

The significance of postoperative mechanical stability to bone repair of comminuted fractures was investigated in an animal experimental study comparing four commonly employed operative methods of fracture stabilization: 1. Plate osteosynthesis combined with lag screw fixation; 2. Bridging plate osteosynthesis; 3. External fixation; 4. Static interlocking intramedullary nailing. As fracture model, a triple wedge osteotomy of the right sheep tibia was used. In regard to biomechanical strength, the method which gave best postoperative stability, plate osteosynthesis in combination with interfragmentary lag screws, did not result in the best bone repair. In this experimental setup, stabilization by bridging methods, inducing bone healing by secondary intention, gave better bone regeneration in the experimental fractures.

Animals↗
PubMed1988

Kinetic evidence for a common binding site for substrates and inhibitors of the neuronal noradrenaline carrier.

The neuronal noradrenaline uptake mechanism (uptake1) has been further characterized. For a number of substrates of uptake1 the half-saturating concentration (Km) and the maximal initial transport rate (Vmax) were determined. Furthermore, the dissociation constants (KD) for binding of these substrates to the desipramine binding site of the neuronal noradrenaline carrier were measured. The uptake experiments were done on rat phaeochromocytoma cells (PC12 cells), the binding experiments on purified plasma membranes of PC12 cells. The substrates differed markedly in respect of Vmax, Km, and KD. Neither Km and Vmax nor KD and Vmax were found to be correlated. However, the discrepancy between Km and KD expressed as the ratio, Km/KD, was negatively correlated with Vmax (r = -0.9315, n = 7, p less than 0.01). For the interpretation of these results a model on the basis of the steady-state assumption has been proposed for uptake1. From the mathematics of that model the following conclusions can be drawn. (1) The half-saturating substrate concentration (Km) is not identical with the dissociation constant for the binding of a substrate to the substrate recognition site (KD). (2) The discrepancy between Km and KD is expected to be negatively correlated with the maximal initial transport rate of the substrate (Vmax). The experimental results are in good agreement with the proposed model for uptake1. Especially the negative correlation between Km/KD and Vmax supports the hypothesis that desipramine inhibits uptake1 via binding to the substrate recognition site of the neuronal noradrenaline carrier.

Adrenal Gland Neoplasms↗