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Biomedical subjects

K Grundmann

Publications and source records attributed to K Grundmann.

9 recordsLinked to original sources
PubMed2003

Aspirin non-responder status in patients with recurrent cerebral ischemic attacks.

BACKGROUND: Antiplatelet agents such as acetylsalicylic acid (aspirin) reduce the relative risk for cerebrovascular events in patients with cardiovascular or cerebrovascular disorders by approximately 23 %. Recent observations raise the possibility that aspirin resistance may contribute to the failure of aspirin treatment in a significant proportion of patients (aspirin non-responders). To evaluate the clinical relevance of aspirin non-responder status, we analysed platelet functions in symptomatic and asymptomatic patients treated with aspirin for secondary prevention of cardiovascular and cerebrovascular events. METHODS: A total of 53 patients on 100 mg aspirin daily for secondary prevention (mean treatment duration > 60 months) were included. Patients were categorized as asymptomatic if they were free of cerebrovascular incidents for at least 24 months (n = 18). Symptomatic patients had suffered ischemic strokes or transient ischemic attacks within the previous 3 days (n = 35). Platelet function was assessed using the PFA-100 system that allows for quantitative assessment of platelet function, reporting platelet aggregatability as the time required to close a small aperture in a biologically active membrane. RESULTS: Collagen/epinephrine closure times were significantly shorter in symptomatic patients than in asymptomatic patients (p < 0.01). Individual closing times were normal in 12 of 35 symptomatic patients (34 % non-responders) whereas all asymptomatic patients had prolonged closure times. CONCLUSIONS: Aspirin non-responder status may contribute to failure of aspirin therapy in the secondary prevention of cerebrovascular incidents in as much as 30-40 % of patients. Quantitative assessment of platelet functions may provide a means to predict aspirin treatment failure in individual patients and to re-direct therapeutic strategies.

Aged↗
PubMed2002

Anatomy during the Third Reich--the Institute of Anatomy at the University of Marburg, as an example.

A complete documentation of German anatomical science and its representatives during the period of national socialism has not been published as yet--contrary to the situation in other medical disciplines. Instead of German anatomists, American anatomists have occasionally addressed this issue during their meetings and have reported on special aspects, such as the use of Nazi symbols in anatomical textbooks and atlases (Pernkopf 1952) and the use of corpses of justice victims for anatomical research and student education. Also, the genesis of the atrocious collection of "racial" skulls, initiated along with the SS-institution of the "Ahnenerbe" by the anatomist August Hirt of Strasbourg (who ordered more than 90 inmates from concentration camps to be murdered in the gas chamber built in the concentration camp of Natzweiler-Struthof close to Strasbourg, Alsace) has been described by Frederic Kasten and others. A broader view of the patterns of behaviour and political actions and fates of contemporary scientists, ranging from dismissal to clandestine opportunism, affirmative cooperation and fanatic activism can be obtained by the analysis of the activities in research, medical education and academic positions of the following members of the Institute of Anatomy at the Philipp-University in Marburg: Ernst Göppert, Eduard Jacobshagen, Ernst-Theodor Nauck, Adolf Dabelow, Helmut Becher and Alfred Benninghoff, whose activities and fates differ in several respects and allow more general deductions. Also, the individual fates of a number of prosecuted Jewish anatomists (Wassermann, München; Poll, Hamburg), of devoted and active members of the Nazi party (Clara, Leipzig; Blotevogel, Breslau) and of criminal fanatics (Hirt, Strasbourg; Kremer, Münster) are briefly discussed. The present contribution is an attempt to initiate a more detailed study of all German departments of anatomy during the Hitler regime and to generate a public discussion among the younger generation of German anatomists.

Anatomy↗
PubMed1999

Twelve novel myosin VIIA mutations in 34 patients with Usher syndrome type I: confirmation of genetic heterogeneity.

Usher syndrome is a heterogeneous autosomal recessive trait and the most common cause of hereditary deaf-blindness. Usher syndrome type I (USH1) is characterised by profound congenital sensorineural hearing loss, vestibular dysfunction, and prepubertal onset of retinitis pigmentosa. Of the at least six different loci for USH1, USH1B maps on chromosome 11q13, and the MYO7A gene has been shown to be defective in USH1B. MYO7A encodes myosin VIIA, an unconventional myosin, and it consists of 48 coding exons. In this study, MYO7A was analysed in 34 unrelated Usher type I patients by single-strand conformation polymorphism analysis and direct sequencing. We identified a total of 12 novel and unique mutations, all single base changes. In addition, we found a previously reported nonsense mutation (C31X) on nine alleles of a total of six patients from Denmark.

Chromosome Mapping↗
PubMed1996

Novel rhodopsin mutation (M216R) in a Danish family with autosomal dominant retinitis pigmentosa.

A novel rhodopsin missense mutation (M216R) was found in a Danish patient with autosomal dominant retinitis pigmentosa. Clinical examination of the proband disclosed a phenotype of intermediate severity. In view of the predicted amino acid substitution in the 5th transmembrane domain of rhodopsin, the clinical picture of the proband is in keeping with the data from the literature on patients carrying similar mutations.

Adolescent↗
PubMed1996

[Not Available].

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Academies and Institutes↗
PubMed1995

[Not Available].

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Anatomy, Comparative↗
PubMed1992

Preservation of hippocampal brain slices with in vivo or in vitro hypothermia.

Hippocampal brain slices show CA1 injury similar to that seen after global ischemia in vivo. Cooling rats to 31 degrees C prior to sacrifice or cooling slices to 21 degrees C for 45 min increased the percentage of normal CA1 pyramidal cells after 5 h in vitro from 30% to over 80%. Brain slices also show a unique, consistent injury in dentate which is lessened by transient cooling to 21 degrees C but not by cooling the animal.

Analysis of Variance↗
PubMed1980

Behaviour of epiphyseal mouse chondrocyte populations in monolayer culture. Morphological and immunohistochemical studies.

Growth and dedifferentiation of a heterogeneous mouse chondrocyte population, prepared from epiphyses of mouse embryos (day 17 of gestation), were studied in primary monolayer culture. At different times of culture, light and electron microscopic investigations were carried out and the change of collagen types was shown by immunofluorescence microscopy. During the first four days in culture, chondrocytes express their typical phenotype. Round or polygonal cells are embedded in a metachromatically staining matrix and produce type II collagen. After four to eight days in vitro most of the chondrocytes lose their matrix capsule and alter to fibroblast-like cells. Simultaneously, a switch of collagen synthesis to type III and type I collagen occurs, whereas the type II collagen synthesis is stopped. Altered cells and transitional stages have intracellular glycogen like typical chondrocytes, but show phagocytosis and indications of cell migration like fibroblasts. It is proposed that these cells, originating from a subpopulation of epiphyseal cartilage, are able to differentiate and dedifferentiate in vitro.

Animals↗