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S Schwarze

Publications and source records attributed to S Schwarze.

3 recordsLinked to original sources
PubMed2002

[Disk-related diseases of the lumbar spine as an example for the critical interaction between clinical diagnosis and occupational disease].

First an overview of the significance of musculoskeletal diseases in terms of national economy and social politics is given, and then the historical development of the occupational disease "disk-related spinal disorders" is outlined. The most important court decisions and the actual state of jurisprudence on this matter are summarized, emphasizing the questions which still have to be answered in the course of medical evaluation of a spinal occupational disease. Based on a joint research project on the spinal effects of whole-body vibrations, an analysis of lumbar X-rays is presented which aimed at detecting specific patterns of response corresponding to the respective extent of strain. In spite of a statistically significant relationship between the clinical diagnosis of a lumbar syndrome and the severity of the degenerative radiological changes on the one hand and vibration exposure on the other hand, the evaluation of the lumbar X-rays did not show any clear radiological pattern related to the exposure. Furthermore, starting points for prevention are discussed. With regard to whole-body vibration, the technical possibilities of reducing the amount of vibration load are still not completely exhausted. However, during preventive measures of occupational health usually carried out as medical screening examinations, the occupational health physician again will face some of the same problems which have already been met with respect to the medical evaluation. Thus, a suggestion is made to modify the traditional concepts of the Professional Industrial Associations on occupational diseases in order to take into account the peculiarities of disk-related spinal disorders.

Accidents, Occupational↗
PubMed2001

Release of non-neuronal acetylcholine from the human placenta: difference to neuronal acetylcholine.

The synthesis and release of non-neuronal acetylcholine, a widely expressed signaling molecule, were investigated in the human placenta. This tissue is free of cholinergic neurons, i.e. a contamination of neuronal acetylcholine can be excluded. The villus showed a choline acetyltransferase (ChAT) activity of 0.65 nmol/mg protein per h and contained 500 nmol acetylcholine/g dry weight. In the absence of cholinesterase inhibitors the release of acetylcholine from isolated villus pieces amounted to 1.3 nmol/g wet weight per 10 min corresponding to a fractional release rate of 0.13% per min. The following substances did not significantly modify the release of acetylcholine: oxotremorine (1 microM), scopolamine (1 microM), (+)-tubocurarine (30 microM), forskolin (30 microM), ouabain (10 microM), 4alpha-phorbol 12,13-didecanoate (1 microM) and tetrodotoxin (1 microM). Removal of extracellular calcium, phorbol 12,13-dibutyrate (1 microM) and colchicine (100 microM) reduced the acetylcholine release between 30% and 50%. High potassium chloride (54 mM and 108 mM) increased the acetylcholine release slightly (by about 30%). A concentration of 10 microM nicotine was ineffective, but 100 microM nicotine enhanced acetylcholine release gradually over a 50-min period without desensitization of the response. The facilitatory effect of nicotine was prevented by 30 microM (+)-tubocurarine. Inhibitors of cholinesterase (physostigmine, neostigmine; 3 microM) facilitated the efflux of acetylcholine about sixfold, and a combination of both (+)-tubocurarine (30 microM) and scopolamine (1 microM) halved the enhancing effect. In conclusion, release mechanisms differ between non-neuronal and neuronal acetylcholine. Facilitatory nicotine receptors are present which are activated by applied nicotine or by blocking cholinesterase. Thus, cholinesterase inhibitors increase assayed acetylcholine by two mechanisms, protection of hydrolysis and stimulation of facilitatory nicotine receptors.

Acetylcholine↗