Intramuscular pressure, tissue oxygenation and EMG fatigue measured during isometric fatigue-inducing contraction of the multifidus muscle.

Simultaneous measurement of intramuscular pressure (IMP), tissue oxygen partial pressure (pO(2)) and EMG fatigue parameters in the multifidus muscle during a fatigue-inducing sustained muscular contraction. The study investigated the following hypotheses: (1) Increases in IMP result in tissue hypoxia; (2) Tissue hypoxia is responsible for loss of function in the musculature. The nutrient supply to muscle during muscle contraction is still not fully understood. It is assumed that muscle contraction causes increased tissue pressure resulting in compromised perfusion and tissue hypoxia. This tissue hypoxia, in turn, leads to muscle fatigue and therefore to loss of function. To the authors' knowledge, no study has addressed IMP, pO(2) and EMG fatigue parameters in the same muscle to gain a deeper sight into muscle perfusion during contraction. As back muscles need to have a constant muscular tension to maintain trunk stability during stance and locomotion, muscle fatigue due to prolonged contraction-induced hypoxia could be an explanation for low back pain. Sixteen healthy subjects performed an isometric muscular contraction exercise at 60% of maximum force until the point of localized muscular fatigue. During this exercise, the individual changes of IMP, pO(2) and the median frequency (MF) of the surface EMG signal of the multifidus muscle were recorded simultaneously. In 12 subjects with a documented increase in intramuscular pressure, only five showed a decrease in tissue oxygen partial pressure, while this parameter remained unchanged in six other subjects and even increased in one. A fall in tissue pO(2) was associated with a drop in MF in only five subjects, while there was no correlation between these parameters in the other 11 subjects. To summarize, an increase in IMP correlated with a decrease in pO(2) and a drop in MF in only five out of 16 subjects. High intramuscular pressure values are not always associated with a hypoxia in muscle tissue. Tissue hypoxia is not automatically associated with a median frequency shift in the EMG signal's power spectrum.

[Accident analytics for structural traumas of the cervical spine]. / Unfallanalytik bei strukturellen Verletzungen der Halswirbelsäule.

The differentiation between degenerative syndromes of the cervical spine and post-traumatic symptoms requires accident analysis. Experiments with human subjects yield data only in the low-energy range, and there are still no accident analyses of structural traumas of the cervical spine. From 1 January 2000 to 30 April 2002, 15 patients with structural injuries to the cervical spine due to car accidents were treated in the Department of Trauma Surgery of the University of Ulm. In 11 of these cases, the DEKRA Ulm completed an appraisal of the accident process.With lateral impacts, structural injuries to the cervical spine can occur even at speeds of only ca 10 km/h. Injuries to the alar ligaments are produced by frontal collisions with substantial differences in speed. Data from accident analysis of structural injuries to the cervical spine must be taken into consideration in causality examinations of distortions of the cervical spine.

A comparative analysis of the interactions of the E6 proteins from cutaneous and genital papillomaviruses with p53 and E6AP in correlation to their transforming potential.

Common necessity for all papillomaviruses is to induce DNA synthesis in quiescent cells. This is commonly achieved by the E7 gene product, which interferes with the function of members of the retinoblastoma family controlling transition from the G1-phase to the S-phase of the cell cycle. Uncontrolled entry into S-phase activates, however, negative growth control signals which have to be bypassed to achieve production of progeny viruses. In addition to inherent activities of the E7 protein, high risk genital types encode an E6 protein that overcomes p53-mediated G1-arrest and apoptosis in concert with the cellular factor E6AP by targeting p53 for the enhanced ubiquitin-dependent degradation. The key question, which of these functions of genital E6 and E7 proteins is responsible for the carcinogenic phenotype, is still not completely answered. In contrast to high risk genital types no immortalizing or transforming activities have been found for the E7 proteins of the high risk cutaneous HPV8 and 47. On the other hand the ability of the E6 protein to transform established rodent fibroblasts seems to be a property shared by high risk genital and cutaneous types. To examine the existence of a common E6-mediated transforming pathway for both virus groups we compared the properties of the cutaneous E6 proteins with already known functions of E6 proteins of genital viruses. For this we analyzed the E6 proteins of low nak and high risk cutaneous and genital papillomaviruses with respect to cell transformation, to their abilities to bind, degradate, and influence the activity of human p53, and to bind E6AP. The results of our study demonstrate a clear lack of interaction between the transforming E6 proteins of HPV1 and HPV8 and both cellular proteins p53 and E6AP. In contrast, we found E6AP-independent binding of HPV16 E6 and HPV6 E6 to p53, although both proteins were different in their transforming potential. Of all four proteins investigated, only HPV16 E6 was able to bind to p53 and E6AP and to induce degradation of the p53 protein in the reticulocyte system. When we investigated in frame deletion mutants of the E6 protein of HPV16 for their abilities to bind to p53 or E6AP, degradate, and inhibit the transactivation function of p53 and to transform rodent fibroblasts, no correlation between the different activities could be found. Mutants still able to bind p53 and E6AP lacked transforming ability and other mutants that were transformation-competent were deficient in p53 and E6AP bindings.