Biomedical subjects

Jürgen Eggers

Publications and source records attributed to Jürgen Eggers.

4 recordsLinked to original sources

PubMed2006

Microemboli in aortic valve replacement.

Microembolic signals (MES) can be detected in many recipients of mechanical aortic valve prostheses by transcranial Doppler ultrasound. The nature and etiology of these MES have remained unclear for a long time. The solid and gaseous nature of MES are discussed, as well as whether or not MES may reflect artifacts. Recently, the gaseous nature of these MES has been widely established. To understand the physics of bubble formation related to mechanical heart valve prostheses, it is necessary to discuss the different types of cavitation occurring at the prostheses and the conditions leading to the degassing of blood. We describe the history of transcranial Doppler ultrasound-techniques and the current techniques in the measurement of these signals. Furthermore, the possible clinical impact of MES, as well as strategies for the design of new prostheses and surgical alternatives to diminish their load are discussed.

Aortic Valve↗

PubMed2005

Sonothrombolysis in acute ischemic stroke for patients ineligible for rt-PA.

The authors studied the effect of transcranial ultrasound on patients with acute middle cerebral artery occlusion and contraindications for thrombolysis. Fifteen consecutive subjects were randomized for insonation over 1 hour or for inclusion in a control group. By day 4, recanalization and neurologic improvement occurred more frequently in the target group. Ultrasound-induced acceleration of clot dissolution may be an option for patients with contraindications for recombinant tissue plasminogen activator.

Acute Disease↗

PubMed2003

Effect of ultrasound on thrombolysis of middle cerebral artery occlusion.

We studied the effect of transcranial 2 MHz Doppler ultrasound (US) on the recanalization and outcome of stroke patients suffering from acute middle cerebral artery occlusion. All patients underwent intravenous recombinant tissue-type plasminogen activator thrombolysis. Eleven patients were randomly selected for continuous US monitoring (C-US) over 1 hour; 14 patients were selected for the control group. The C-US group showed a higher grade of recanalization after 1 hour but also a higher number of intraparenchymal bleedings. Overall, a favorable functional outcome occurred more frequently in the C-US group (Barthel index, p = 0.037) after 3 months.

Brain↗

PubMed2002

Residual galactosylsphingosine (psychosine) beta-galactosidase activities and associated GALC mutations in late and very late onset Krabbe disease.

BACKGROUND: Krabbe disease (globoid-cell leukodystrophy; GLD) is caused by mutations in the GALC gene. Beta-galactocerebrosidase (GALC) is a specific beta-galactosidase which is defective in GLD. About 90% of GLD patients have an infantile course by fatal cerebral demyelination, but 10% have a later onset (LOGLD) of symptoms and survive for one or several decades. METHODS: Activities of GALC towards galactosylceramide (GC) and galactosylsphingosine (psychosine; PS) were determined in white blood cells and cultured fibroblasts derived from GLD patients and controls using tritium-labelled natural substrates. In the galactosylsphingosine (psychosine) beta-galactosidase (GALC-PS) assay, a thin layer chromatographic technique was used to separate enzymatically released radioactive galactose. RESULTS: Both galactosylceramide beta-galactosidase (GALC-GC) and GALC-PS activities were reduced by at least 85% of the normal in all but 2 of the 10 GLD patients studied. In particular, one 23-year-old severely demyelinated LOGLD patient was strongly deficient (11% of the normal) in GALC-GC but apparently normal for GALC-PS activity. This patient's GALC genotype was the 30-kb-deleted/502T allele combined with a wild-type allele in the 1637C background known to slightly reduce GALC-GC activity. Further, of six LOGLD patients, both of 62- and 63-year-old brothers had the deleted allele combined with an 809G>A mutated 1637C allele. The sibs had strongly reduced GALC-GC and GALC-PS activities but became clinically remarkable only in their 50s with a severe mental downhill course in one of them. CONCLUSIONS: A GALC genotype with one deleted and one polymorphic GALC activity-reducing allele can lead to enzymatic and clinical signs of LOGLD in the absence of marked GALC-PS deficiency. If an active PS hydrolysis in the fibroblasts of a LOGLD patient also reflected such hydrolysis in the brain, the psychosine hypothesis for GLD may need to be revised.

Age of Onset↗