[Chances and Potential of a Modern Surgical Skills Lab as Substantial Practical Part of the Study of Human Medicine - "The Magdeburg Model"]. / Chancen und Potenziale eines modernen chirurgisch geprägten SkillsLabs im Rahmen des Humanmedizinstudiums ­ das Magdeburger Modell.

Introduction: Surgical education of medical students within "skills labs" have not been standardised throughout Germany as yet; there is a substantial impact of available aspects such as personal and space at the various medical schools. Aim: The aim of this contribution is to illustrate the concept of a surgical skills lab in detail, including curricular teaching and integrated facultative courses at the Medical School, University of Magdeburg ("The Magdeburg Model") in the context of a new and reconstructed area for the skills lab at the Magdeburg's apprenticeship center for medical basic abilities (MAMBA). Method: We present an overview on the spectrum of curricular and facultative teaching activities within the surgical part of the skills lab. Student evaluation of this teaching concept is implemented using the programme "EvaSys" and evaluation forms adapted to the single courses. Results: By establishing MAMBA, the options for a practice-related surgical education have been substantially improved. Student evaluations of former courses presented within the skills lab and the chance of moving the skills lab into a more generous and reconstructed area led to a reorganisation of seminars and courses. New additional facultative courses held by student tutors have been introduced and have shown to be of great effect, in particular, because of their interdisciplinary character. Conclusion: Practice-related surgical education within a skills lab may have the potential to effectively prepare medical students for their professional life. In addition, it allows one to present and teach the most important basic skills in surgery, which need to be pursued by every student. An enthusiastic engagement of the Office for Student Affairs can be considered the crucial and indispensable link between clinical work and curricular as well as facultative teaching with regard to organisation and student evaluation. The practice-related teaching parts and contents at the surgical section of a skills lab should be integrated into the National Competence-based Catalogue of Teaching Aims in Medicine ("NKLM").

Absence of major accumulation of mitochondrial ND5 mutations in Parkinson patient muscle.

UNLABELLED: The pathogenesis of the selective loss of dopaminergic neurons in idiopathic Parkinson's disease (PD) has not been understood up to now. Respiratory chain dysfunction and accumulation of mitochondrial DNA deletions to biochemically relevant levels have been observed in the dopaminergic neurons. However, respiratory chain defects have also been reported in other tissues, pointing to a generalized component of oxidative stress in PD. Recently, somatic point mutations in a narrow region of the complex I polypeptide ND5 (codons 120 - 150) were suggested to separate PD patients from age-matched controls, using frontal cortex homogenates. OBJECTIVE: The present study intended to analyze whether those recently described ND5 mutations may also generally occur in skeletal muscle tissue of PD patients, in which complex I dysfunction had been measured earlier with biochemical approaches. MATERIAL: Skeletal muscle biopsy samples of 5 PD individuals with a previously characterized biochemical complex I defect and of 5 age-matched controls were used. METHOD: DNA was extracted from the muscle samples. The relevant ND5 region was PCR-cloned using a high fidelity Pfu polymerase and a low number of PCR cycles (15). Amean number of 96 clones were randomly selected from the ampicillin plates and sequenced by the dye terminator method to allow the detection of low abundance mutations with a sensitivity around 1%. RESULTS: Mutations between codons 120 and 150 were only slightly more frequent in PD versus controls (60 versus 40% of samples affected), while this ratio had been 100 versus 12.5% in frontal cortex. CONCLUSIONS: In contrast to results reported for PD frontal cortex, low-level ND5 mutations between codons 120 and 150 do not accumulate severely in biochemically affected skeletal muscle samples of PD patients.

Glutathione depletion in antioxidant defense of differentiated NT2-LHON cybrids.

The mechanism of retinal ganglion cell loss in Leber's hereditary optic neuropathy (LHON) is still uncertain, and a role of enhanced superoxide production by the mutant mitochondrial complex I has been hypothesized. In the present study, it was shown that LHON cybrids, carrying the np11778 mutation, became selectively more H(2)O(2) sensitive compared with the parental cell line only following short-term retinoic acid differentiation. They contained a decreased cellular glutathione pool (49%, p< or =0.05), despite 1.5-fold enhanced expression of the regulatory subunit of gamma-glutamylcysteine synthetase (p< or =0.05). This points to a reduction of the capacity to detoxify H(2)O(2) and to changes in thiol redox potential. The activity of the H(2)O(2) degrading enzyme glutathione peroxidase (GPx) and the activities of glutathione reductase (GR) and superoxide dismutase (SOD) were unaffected.

Re-evaluation of the dysfunction of mitochondrial respiratory chain in skeletal muscle of patients with Parkinson's disease.

The origin and tissue distribution of the mitochondrial dysfunction in Parkinson's disease (PD) remains still a matter of controversy. To re-evaluate a probably free radical-born, generalized mitochondrial impairment in PD, we applied optimized enzymatic assays, high resolution oxygraphic measurements of permeabilized muscle fibers, and application of metabolic control analysis to skeletal muscle samples of 19 PD patients and 36 age-matched controls. We detected decreased activities of respiratory chain complexes I and IV being accompanied by increased flux control coefficients of complexes I and IV on oxygen consumption of muscle fibers. We further investigated if randomly distributed point mutations in two discrete regions of the mitochondrial DNA are increased in PD muscle, and if they could contribute to the mitochondrial impairment. Our data confirm the previously debated presence of a mild mitochondrial defect in skeletal muscle of patients with PD which is accompanied with an about 1.5 to 2-fold increase of point mutated mtDNA.