Biomedical subjects

W Seeger

Publications and source records attributed to W Seeger.

400 records · Page 23Linked to original sources

PubMedDate not supplied

[Reduction of radiation exposure in full spine images in youth].

With a phantom of the vertebral column in 16 measuring series using diagnostic dosimeters the influence of grid, recording voltage, focus-film distance (FFD) and film-foil-systems on the radiation exposure was examined. With identical film-foil systems this resulted in a dose reduction by a factor of 4 to 7 for X-rays without grid compared to X-rays using grid. Therefore in case of follow-ups with questions about the statics of the vertebral column it is recommended to X-rays without grid. The studies can substantiate also the recommendations aiming at the avoidance of long exposure times to apply small mAs-products and voltages as high possible, to use highly sensitive film-screen systems (e.g. EU 600) and not to exceed a FFD of 2 m). These actions even when used separately and certainly when used simultaneously cause a considerable cut in radiation exposure. A radiation exposure decreasing effect is given by taking total X-rays compared to partial X-rays which is appropriate especially with slim patients.

Adolescent↗

PubMedDate not supplied

Septic lung.

"Septic lung" is a variant of the acute respiratory distress syndrome. The key alterations of this syndrome are an increase in pulmonary vascular resistance and a diffuse increase in pulmonary vascular permeability, with subsequent formation of protein-rich interstitial and intraalveolar edema, disturbance of alveolar surfactant function, and severe impairment of gas exchange. In a model of blood-free perfused rabbit lungs, all these alterations in pulmonary physiology are mimicked by stimulation of the pulmonary vascular arachidonic acid (AA) cascade: increased pulmonary artery pressure is predominantly caused by the AA cyclooxygenase product thromboxane A2, whereas vascular leakage must be ascribed to the stimulation of the various AA lipoxygenase pathways. This local lipid-mediator system in the pulmonary vasculature is directly triggered by bacterial protein toxins such as Staphylococcus aureus alpha toxin and Pseudomonas aeruginosa cytotoxin, which start the AA cascade by serving as nonphysiologic calcium-bypass gates in cellular membranes. Moreover, bacteremia and endotoxemia may be effective via activation of the classical humoral cascade systems and leukocyte stimulation, which are all linked to the AA cascade in the pulmonary circulation as a common final pathway.

Animals↗

PubMedDate not supplied

Staphylococcal alpha-toxin provokes coronary vasoconstriction and loss in myocardial contractility in perfused rat hearts: role of thromboxane generation.

BACKGROUND: Cardiac performance is severely depressed in septic shock. Endotoxin has been implicated as the causative agent in Gram-negative sepsis, but similar abnormalities are encountered in Gram-positive sepsis. We investigated the influence of the major exotoxin of Staphylococcus aureus, staphylococcal alpha-toxin, in isolated perfused rat hearts. METHODS AND RESULTS: Alpha-toxin 0.25 to 1 microg/mL caused a dose-dependent increase in coronary perfusion pressure that more than doubled. In parallel, we noted a decrease in left ventricular developed pressure and the maximum rate of left ventricular pressure rise (dP/dt(max)), dropping to a minimum of <60% of control. These changes were accompanied by a liberation of thromboxane A(2) and prostacyclin into the coronary effluent. The release of creatine kinase, lactate dehydrogenase, potassium, and lactate did not surpass control heart values, and leukotrienes were also not detected. Indomethacin, acetylsalicylic acid, and the thromboxane receptor antagonist daltroban fully blocked the alpha-toxin-induced coronary vasoconstrictor response and the decrease in left ventricular developed pressure and dP/dt(max), whereas the lipoxygenase inhibitor nordihydroguaiaretic acid, the platelet activating factor antagonist WEB 2086, and the alpha-adrenergic antagonist phentolamine were entirely ineffective. Inhibition of nitric oxide synthase even enhanced the alpha-toxin-induced increase in coronary perfusion pressure and the loss in myocardial performance. CONCLUSIONS: Purified staphylococcal alpha-toxin provokes coronary vasoconstriction and loss in myocardial contractility. The responses appear to be largely attributable to the generation of thromboxane and are even enhanced when the endogenous nitric oxide synthesis is blocked. Bacterial exotoxins, such as staphylococcal alpha-toxin, may thus be implicated in the loss of cardiac performance encountered in Gram-positive septic shock.

Animals↗

PubMedDate not supplied

Synthesis and studies on the biophysical activity of human lung surfactant peptide SP-C and its N-terminal fragments.

Human lung surfactant peptide SP-C and two of its N-terminal fragments were prepared by SPPS and their biophysical activities investigated in vitro using a pulsating bubble surfactometer. These studies demonstrated that even low doses of the synthetic peptides with the natural human sequence of SP-C in combination with reconstituted lipid mixtures causes a drastic decrease of surface tension.

Amino Acid Sequence↗