Effects of electro-mechanical uncouplers, hormonal stimulation and pacing rate on the stability and function of cultured rabbit myocardial slices.

Introduction: Recent advances have enabled organotypic culture of beating human myocardial slices that are stable for weeks. However, human myocardial samples are rare, exhibit high variability and frequently originate from diseased hearts. Thus, there is a need to adapt long-term slice culture for animal myocardium. When applied to animal cardiac slices, studies in healthy or genetically modified myocardium will be possible. We present the culture of slices from rabbit hearts, which resemble the human heart in microstructure, electrophysiology and excitation-contraction coupling. Methods: Left ventricular myocardium from New Zealand White rabbits was cut using a vibratome and cultured in biomimetic chambers for up to 7 days (d). Electro-mechanical uncoupling agents 2,3-butanedione monoxime (BDM) and cytochalasin D (CytoD) were added during initiation of culture and effects on myocyte survival were quantified. We investigated pacing rates (0.5 Hz, 1 Hz, and 2 Hz) and hormonal supplements (cortisol, T3, catecholamines) at physiological plasma concentrations. T3 was buffered using BSA. Contractile force was recorded continuously. Glucose consumption and lactate production were measured. Whole-slice Ca2+ transients and action potentials were recorded. Effects of culture on microstructure were investigated with confocal microscopy and image analysis. Results: Protocols for human myocardial culture resulted in sustained contracture and myocyte death in rabbit slices within 24 h, which could be prevented by transient application of a combination of BDM and CytoD. Cortisol stabilized contraction amplitude and kinetics in culture. T3 and catecholaminergic stimulation did not further improve stability. T3 and higher pacing rates increased metabolic rate and lactate production. T3 stabilized the response to ß-adrenergic stimulation over 7 d. Pacing rates above 1 Hz resulted in progredient decline in contraction force. Image analysis revealed no changes in volume fractions of cardiomyocytes or measures of fibrosis over 7 d. Ca2+ transient amplitudes and responsiveness to isoprenaline were comparable after 1 d and 7 d, while Ca2+ transient duration was prolonged after 7 d in culture. Conclusions: A workflow for rabbit myocardial culture has been established, preserving function for up to 7 d. This research underscores the importance of glucocorticoid signaling in maintaining tissue function and extending culture duration. Furthermore, BDM and CytoD appear to protect from tissue damage during the initiation phase of tissue culture.

Conservative Solitons and Reversibility in Time Delayed Systems.

Time delayed dynamical systems have proven to be a fertile framework for the study of physical phenomena. In natural sciences, their uses have been limited to the study of dissipative dynamics. In this Letter, we demonstrate the existence of nonlinear reversible conservative time delayed systems. We consider the example of a dispersive microcavity containing a Kerr medium coupled to a distant external mirror. At low energies and in the long delay limit, a multiscale analysis shows the equivalence with the nonlinear Schrödinger equation. We unveil some of the symmetries and conserved quantities, as well as bright temporal solitons. While elastic collisions occur for shallow wave packets, we observe the lack of integrability at higher energies. We recover the Lugiato-Lefever equation in the weakly dissipative regime.

Manipulation of temporal localized structures in a vertical external-cavity surface-emitting laser with optical feedback.

We analyze the effect of optical feedback on the dynamics of an external-cavity passively mode-locked surface-emitting laser operating in the regime of temporal localized structures. Depending on the ratio between the cavity round trip time and the feedback delay, we show experimentally that feedback acts as a solution selector that either reinforces or hinders the appearance of one of the multistable harmonic arrangements of pulses. Our theoretical analysis reproduces well the experiment and allows us to evidence asymmetrical resonance tongues due to the parity symmetry-breaking induced by gain depletion.

Diagnostic contribution of individual components of adrenal function tests to diagnose canine hyperadrenocorticism.

There is limited information regarding the value of constitutive components of the ACTH stimulation test (ACTHST) and low-dose dexamethasone suppression test (LDDST) including serum baseline cortisol (BC), difference between post-ACTH stimulation cortisol (PC) and BC (ΔACTHC), cortisol concentration 4h after dexamethasone administration (4HC), difference between 4HC and BC (Δ4C), and the difference between cortisol concentration 8h after dexamethasone administration and 4HC (Δ8C). Therefore, the objective of this study was to determine if these components can predict hyperadrenocorticism, pituitary-dependent hyperadrenocorticism (PDH), or functional adrenocortical tumor (FAT) in dogs. Cortisol concentrations were normalized, as fold change (FC), to the PC reference interval upper limit. A total of 1267 dogs were included, with hyperadrenocorticism diagnosed in 537 (PDH, n=356; FAT, n=28; undetermined, n=153) and excluded in 730. The area under the receiver operating curves for BC, ΔACTHC, 4HC, Δ4C, and Δ8C to predict hyperadrenocorticism were 0.76 (95% confidence interval (CI), 0.73-0.79), 0.91 (95% CI, 0.89-0.93), 0.83 (95% CI, 0.80-0.87), 0.55 (95% CI, 0.50-0.60), and 0.67 (95% CI, 0.62-0.72), respectively. A diagnostic limit of ≥0.78 FC for ΔACTHC had excellent sensitivity (1.00; 95% CI, 0.74-1.00), but poor specificity (0.67; 95% CI, 0.64-0.71), to predict FAT in dogs with a positive ACTHST. A diagnostic limit of ≥-0.26 FC for Δ4C had excellent sensitivity (1.00; 95% CI, 0.79-1.00), but poor specificity (0.21; 95% CI, 0.18-0.26), to predict FAT in dogs with a positive LDDST. In hyperadrenocorticoid dogs that have positive ACTHST or LDDST results, ΔACTHC or Δ4C, respectively, could be used to exclude FAT.

Remodeling of the transverse tubular system after myocardial infarction in rabbit correlates with local fibrosis: A potential role of biomechanics.

The transverse tubular system (t-system) of ventricular cardiomyocytes is essential for efficient excitation-contraction coupling. In cardiac diseases, such as heart failure, remodeling of the t-system contributes to reduced cardiac contractility. However, mechanisms of t-system remodeling are incompletely understood. Prior studies suggested an association with altered cardiac biomechanics and gene expression in disease. Since fibrosis may alter tissue biomechanics, we investigated the local microscopic association of t-system remodeling with fibrosis in a rabbit model of myocardial infarction (MI). Biopsies were taken from the MI border zone of 6 infarcted hearts and from 6 control hearts. Using confocal microscopy and automated image analysis, we quantified t-system integrity (ITT) and the local fraction of extracellular matrix (fECM). In control, fECM was 18 ± 0.3%. ITT was high and homogeneous (0.07 ± 0.006), and did not correlate with fECM (R2 = 0.05 ± 0.02). The MI border zone exhibited increased fECM within 3 mm from the infarct scar (30 ± 3.5%, p < 0.01 vs control), indicating fibrosis. Myocytes in the MI border zone exhibited significant t-system remodeling, with dilated, sheet-like components, resulting in low ITT (0.03 ± 0.008, p < 0.001 vs control). While both fECM and t-system remodeling decreased with infarct distance, ITT correlated better with decreasing fECM (R2 = 0.44) than with infarct distance (R2 = 0.24, p < 0.05). Our results show that t-system remodeling in the rabbit MI border zone resembles a phenotype previously described in human heart failure. T-system remodeling correlated with the amount of local fibrosis, which is known to stiffen cardiac tissue, but was not found in regions without fibrosis. Thus, locally altered tissue mechanics may contribute to t-system remodeling.

Analyzing Remodeling of Cardiac Tissue: A Comprehensive Approach Based on Confocal Microscopy and 3D Reconstructions.

Microstructural characterization of cardiac tissue and its remodeling in disease is a crucial step in many basic research projects. We present a comprehensive approach for three-dimensional characterization of cardiac tissue at the submicrometer scale. We developed a compression-free mounting method as well as labeling and imaging protocols that facilitate acquisition of three-dimensional image stacks with scanning confocal microscopy. We evaluated the approach with normal and infarcted ventricular tissue. We used the acquired image stacks for segmentation, quantitative analysis and visualization of important tissue components. In contrast to conventional mounting, compression-free mounting preserved cell shapes, capillary lumens and extracellular laminas. Furthermore, the new approach and imaging protocols resulted in high signal-to-noise ratios at depths up to 60 µm. This allowed extensive analyzes revealing major differences in volume fractions and distribution of cardiomyocytes, blood vessels, fibroblasts, myofibroblasts and extracellular space in control vs. infarct border zone. Our results show that the developed approach yields comprehensive data on microstructure of cardiac tissue and its remodeling in disease. In contrast to other approaches, it allows quantitative assessment of all major tissue components. Furthermore, we suggest that the approach will provide important data for physiological models of cardiac tissue at the submicrometer scale.

Identification of the putative binding pocket of valerenic acid on GABAA receptors using docking studies and site-directed mutagenesis.

BACKGROUND AND PURPOSE: ß2/3-subunit-selective modulation of GABAA receptors by valerenic acid (VA) is determined by the presence of transmembrane residue ß2/3N265. Currently, it is not known whether ß2/3N265 is part of VA's binding pocket or is involved in the transduction pathway of VA's action. The aim of this study was to clarify the localization of VA's binding pocket on GABAA receptors. EXPERIMENTAL APPROACH: Docking and a structure-based three-dimensional pharmacophore were employed to identify candidate amino acid residues that are likely to interact with VA. Selected amino acid residues were mutated, and VA-induced modulation of the resulting GABAA receptors expressed in Xenopus oocytes was analysed. KEY RESULTS: A binding pocket for VA at the ß(+) /α(-) interface encompassing amino acid ß3N265 was predicted. Mutational analysis of suggested amino acid residues revealed a complete loss of VA's activity on ß3M286W channels as well as significantly decreased efficacy and potency of VA on ß3N265S and ß3F289S receptors. In addition, reduced efficacy of VA-induced IGABA enhancement was also observed for α1M235W, ß3R269A and ß3M286A constructs. CONCLUSIONS AND IMPLICATIONS: Our data suggest that amino acid residues ß3N265, ß3F289, ß3M286, ß3R269 in the ß3 subunit, at or near the etomidate/propofol binding site(s), form part of a VA binding pocket. The identification of the binding pocket for VA is essential for elucidating its pharmacological effects and might also help to develop new selective GABAA receptor ligands.

The intubation scoop (i-scoop) - a new type of laryngoscope for difficult and normal airways.

The i-scoop is an intubation device with a curved guiding bar with laterally located lenses at its tip, rather than a blade. Twenty-five anaesthesiologists intubated a manikin that simulated first a normal and then a difficult airway. All participants were able to intubate the difficult airway with a good view of the glottis using the i-scoop. None was able to intubate using seven other laryngoscopes (Macintosh laryngoscope, GlideScope(®) GVL and AVL, McGrath(®) (Series 5/MAC), C-MAC(®) , A.P. Advance(™) ). Intubation was successful only with the Airtraq(®) (n = 10), the Airway Scope (n = 5), the C-MAC D-Blade (n = 2), the A.P. Advance DAB (n = 1) and the GlideScope DL Trainer (n = 1) (p < 0.001, success rate of i-scoop vs all 12 laryngoscopes combined). In contrast to all other videolaryngoscopes, intubation of the normal airway with the i-scoop was achieved even faster than with the Macintosh laryngoscope (p < 0.02). The i-scoop outperformed all other laryngoscopes in both difficult and normal airways, and therefore has potential as an easier and safer alternative to present devices.

Effects of metoprolol therapy on cardiac gap junction remodelling and conduction in human chronic atrial fibrillation.

BACKGROUND AND PURPOSE: We investigated the influence of metoprolol on gap junction proteins connexin43 (Cx43) and connexin40 (Cx40) in atrial tissue from patients with/without atrial fibrillation (AF). EXPERIMENTAL APPROACH: Left atrial tissue samples from 160 patients with AF or sinus rhythm (SR) with or without metoprolol (mean daily dose: 65.2 ± 9.1 mg·day⁻¹) were analysed for Cx43 and Cx40 by Western blot and immunohistology. Transverse and longitudinal conduction velocities were determined by 64 multi-electrode mapping. KEY RESULTS: Both Cx43 and Cx40 expression were significantly increased in patients with AF versus SR. Cx43-expression in AF was significantly higher in patients receiving metoprolol, while Cx40 expression was unaffected by metoprolol treatment. In AF, the ratio of lateral/polar expression of Cx43 and Cx40 was enhanced due to increased expression at the sides of the cells (lateral) and a loss at the cell poles. This AF-induced increase in lateral/polar expression of Cx43, but not of Cx40, was significantly antagonized by metoprolol treatment. Functionally, in AF patients, transverse conduction velocity in atrial samples was significantly enhanced and this change was also significantly antagonized by metoprolol. CONCLUSIONS AND IMPLICATIONS: AF induced enhanced lateral expression of Cx43 and Cx40 together with enhanced transverse conduction velocity in left atrial tissue. Alterations in localization of Cx43 and conduction changes were both antagonized by metoprolol, showing that pharmacological modulation of gap junction remodelling seems, in principle, possible. This finding may open new approaches to the development of anti-arrythmic drugs.

Age related changes in mitochondrial function and new approaches to study redox regulation in mammalian oocytes in response to age or maturation conditions.

Mammalian oocytes are long-lived cells in the human body. They initiate meiosis already in the embryonic ovary, arrest meiotically for long periods in dictyate stage, and resume meiosis only after extensive growth and a surge of luteinizing hormone which mediates signaling events that overcome meiotic arrest. Few mitochondria are initially present in the primordial germ cells while there are mitogenesis and structural and functional differentiation and stage-specific formation of functionally diverse domains of mitochondria during oogenesis. Mitochondria are most prominent cell organelles in oocytes and their activities appear essential for normal spindle formation and chromosome segregation, and they are one of the most important maternal contributions to early embryogenesis. Dysfunctional mitochondria are discussed as major factor in predisposition to chromosomal nondisjunction during first and second meiotic division and mitotic errors in embryos, and in reduced quality and developmental potential of aged oocytes and embryos. Several lines of evidence suggest that damage by oxidative stress/reactive oxygen species in dependence of age, altered antioxidative defence and/or altered environment and bi-directional signaling between oocyte and the somatic cells in the follicle contribute to reduced quality of oocytes and blocked or aberrant development of embryos after fertilization. The review provides an overview of mitogenesis during oogenesis and some recent data on oxidative defence systems in mammalian oocytes, and on age-related changes as well as novel approaches to study redox regulation in mitochondria and ooplasm. The latter may provide new insights into age-, environment- and cryopreservation-induced stress and mitochondrial dysfunction in oocytes and embryos.

MCAK is present at centromeres, midspindle and chiasmata and involved in silencing of the spindle assembly checkpoint in mammalian oocytes.

Mitotic centromere-associated kinesin (MCAK) is an ATP-dependent microtubule (MT) depolymerase regulated by Aurora kinase (AURK) phosphorylation and implicated in resolution of improper MT attachments in mitosis. Distribution of MCAK was studied in oocyte maturation by anti-MCAK antibody, anti-tubulin antibody, anti-AURKB antibody and anti-centromere antibody (ACA) and by the expression of MCAK-enhanced green fluorescent protein fusion protein in maturing mouse oocytes. Function was assessed by knockdown of MCAK and Mad2, by inhibiting AURK or the proteasome, by live imaging with polarization microscope and by chromosomal analysis. The results show that MCAK is transiently recruited to the nucleus and transits to spindle poles, ACA-positive domains and chiasmata at prometaphase I. At metaphase I and II, it is present at centrosomes and centromeres next to AURKB and checkpoint proteins Mad2 and BubR1. It is retained at centromeres at telophase I and also at the midbody. Knockdown of MCAK causes a delay in chromosome congression but does not prevent bipolar spindle assembly. MCAK knockdown also induces a meiosis I arrest, which is overcome by knockdown of Mad2 resulting in chiasma resolution, chromosome separation, formation of aberrant meiosis II spindles and increased hypoploidy. In conclusion, MCAK appears to possess a unique distribution and function in oocyte maturation. It is required for meiotic progression from meiosis I to meiosis II associated with silencing of the spindle assembly checkpoint. Alterations in abundance and activity of MCAK, as implicated in aged oocytes, may therefore contribute to the loss of control of cell cycle and chromosome behaviour, thus increasing risk for errors in chromosome segregation and aneuploidy.

Treatment during primary HIV infection does not lower viral set point but improves CD4 lymphocytes in an observational cohort.

OBJECTIVE: To investigate if early treatment of primary HIV-1 infection (PHI) reduces viral set point and/or increases CD4 lymphocytes. METHODS: Analysis of two prospective multi-centre PHI cohorts. HIV-1 RNA and CD4 lymphocytes in patients with transient treatment were compared to those in untreated patients. Time to CD4 lymphocyte decrease below 350/ microl after treatment stop or seroconversion was calculated using Kaplan-Meier and Cox-PH-regression analyses. RESULTS: 156 cases of PHI were included, of which 100 had received transient HAART (median treatment time 9.5 months) and 56 remained untreated. Median viral load (563000 cop/ml vs 240000 cop/ml; p<0.001) and median CD4 lymphocyte (449/ microl vs. 613/ microl; p<0.01) differed significantly between treated and untreated patients. Median viral load was 38056 copies/ml in treated patients (12 months after treatment stop) and 52880 copies/ml in untreated patients (12 months after seroconversion; ns). Median CD4 lymphocyte change was +60/ microl vs. -86/ microl (p = 0.01). Median time until CD4 lymphocytes decreased to <350/ microl (including all patients with CD4 lymphocytes <500/ microl during seroconversion) was 20.7 months in treated patients after treatment stop and 8.3 months in untreated patents after seroconversion (p<0.01). Cox-PH analyses adjusting for baseline VL, CD4 lymphocytes, stage of early infection and symptoms confirmed these differences. CONCLUSIONS: Treatment during PHI did not lower viral set point. However, patients treated during seroconversion had an increase in CD4 lymphocytes, whereas untreated patients experienced a decrease in CD4 lymphocytes. Time until reaching CD4 lymphocytes <350/ microl was significantly shorter in untreated than in treated patients including patients with CD4 lymphocytes <500/ microl during seroconversion.

[Occupational and non-occupational risk factors in bladder cancer patients in an industrialized area located in former East-Germany]. / Berufliche und ausserberufliche Risikofaktoren für das Harnblasenkarzinom in einem ehemaligen Industriegebiet der neuen Bundesländer.

PURPOSE: Several occupational carcinogens are metabolized by polymorphic enzymes. The distribution of the polymorphic enzymes N-acetyltransferase 2 (NAT2; substrates: aromatic amines), glutathione S-transferase M1 (GSTM1; substrates: e. g., reactive metabolites of polycyclic aromatic hydrocarbons), and glutathione S-transferase T1 (GSTT1; substrates: small molecules with 1 - 2 carbon atoms) were investigated. MATERIAL AND METHODS: At the urological department in Lutherstadt Wittenberg, 136 patients with a histologically proven transitional cell cancer of the urinary bladder were investigated for all occupations performed for more than 6 months. Several occupational and non-occupational risk factors were asked. The genotypes of NAT2, GSTM1, and GSTT1 were determined from leucocyte DNA by PCR. RESULTS: Compared to the general population in Middle Europe, the percentage of GSTT1 negative persons (22.1 %) was ordinary; the percentage of slow acetylators (59.6 %) was in the upper normal range, while the percentage of GSTM1 negative persons (58.8 %) was elevated in the entire group. Shifts in the distribution of the genotypes were observed in subgroups who had been exposed to asbestos (6/6 GSTM1 negative, 5/6 slow acetylators), rubber manufacturing (8/10 GSTM1 negative), and chlorinated solvents (9/15 GSTM1 negative). CONCLUSIONS: The overrepresentation of GSTM1 negative bladder cancer patients also in this industrialized area and more pronounced in several occupationally exposed subgroups points to an impact of the GSTM1 negative genotype in bladder carcinogenesis.

Ambulatory electrogastrography in patients with sclerodermia, delayed gastric emptying, dyspepsia, and irritable bowel syndrome. Is there any clinical relevance?

Background: Changes in electrogastrographic parameters are described in patients with irritable bowel syndrome, sclerodermia, dyspepsia, and delayed gastric emptying in static measurements. However, no information is available about changes in ambulatory measurements. The objective of this study was to find parameters that discriminate between these diseases using cutaneous 24-h-electrogastrography. Methods: Cutaneous 24-h electrogastrography (EGG) measurements were taken from 20 patients with dyspepsia, 10 patients with systemic sclerosis (sclerodermia, SSc), 7 patients with irritable bowel syndrome (IBS), 7 patients with delayed gastric emptying, and 10 healthy volunteers. Measurements were made using a DIGITRAPPER EGG (Synectics Medical Inc., Stockholm, Sweden) and the accompanying computerized data analysis package (ElectroGastroGram Version 6.30, Gastrosoft Inc., Synectics Medical Inc., Stockholm, Sweden). Frequency and power were compared pre- and postprandially, as well as during the entire day of measurement. Results: The 24-h measurements in healthy volunteers revealed 45.00%+/-12.12% normal values (2.4-3.7 cpm), 30.10%+/-7.15% bradygastric values (<2.4 cpm), and 24.20%+/-7.76% tachygastric values (>3.7 cpm). There was no significant change in frequency between rest and motion, but there was a significant increase in power (P<0.05). There was significantly more bradygastria in patients with dyspepsia periprandially as well as after 24 h (P<0.01) than in healthy volunteers. The mean power of patients with dyspepsia was significantly higher than that of patients with IBS (P<0.05). Conclusion: Cutaneous 24-h-EGG may be used as an additional means of differentiating between dyspepsia and IBS.

Tropheryma whippelii DNA in saliva of patients without Whipple's disease.

Tropheryma whippelii is the causative agent of Whipple's disease, a difficult to diagnose systemic illness. Amplification of part of its 16S ribosomal RNA gene(s) has become a standard diagnostic method because of increased sensitivity as compared to classical histopathological analysis. Recently, we demonstrated the presence of T. whippelii DNA by PCR in duodenal biopsies and/or gastric juice of a considerable fraction of individuals without clinical signs of Whipple's disease. In this follow-up study, saliva and dental plaques of the same patients were screened for the presence of T. whippelii DNA. Six out of the 14 previously PCR-positive persons but none of the 17 controls had T. whippelii DNA in their saliva. Our results suggest that Whipple bacteria are ubiquitous environmental or commensal organisms causing Whipple's disease only in a particular subset of individuals, possibly those with an as yet uncharacterized immunological defect.

[Treatment of scoliosis and scoliokyphosis in Recklinghausen neurofibromatosis]. / Behandlung der Skoliose und Skoliokyphose bei Neurofibromatosis Recklinghausen (NF).

Spine deformities are a frequent symptom of neurofibromatosis Recklinghausen. Especially NF1 shows next to numerous alterations in the skeleton in some cases massive scoliosis and kyphosis. There are different theories for the development of the spine deformities, one of them is that specific alterations of the vertebra are caused by an elevated intraspinal pressure on the osteoporotic bone. A classification from a clinical point of view discriminates 3 types of severity. Type 1 shows instead of the in x-rays inconspicuous findings neurofibromatosistypical alterations in other diagnostic procedures (e.g. MRI). Extreme variations like short curved scoliokyphosis with massive destruction and severe spine imbalance are described as type 3. Operative treatment is dependent on the severity of the deformity. Intraspinal tumors have to be removed. Because of the elevated neurological risk the proceeding has to be very careful, sometimes there is a temporary Halo-extension necessary. Anterior substance defects are filled with bone or cages. The posterior instrumentation (in most of the cases a 2-rod-stabilization) is performed by transpedicular screws. Frequently there is a concave chest wall plastic (CTP) indicated. To prevent neurological complications early surgical procedure is sometimes necessary. Complications can be reduced by careful proceeding, exact preoperative diagnostic and classification. But next to operative experience a qualified anaesthesiological and intensive care units are absolutely necessary.

[Efficacy of ultrasound controlled direct reposition of fragments of the posterior vertebral body facet]. / Die Effizienz der sonographisch kontrollierten direkten Reposition von Fragmenten der Wirbelkörperhinterkante.

To calculate canal compromise and decrease of midsagittal diameter caused by retropulsion of fragments into the spinal canal we analyzed the pre- and postoperative computed tomographies of 32 patients with unstable thoracolumbar burst fractures treated by USS (universal spine system). Our intention was to examine the efficiency of ultrasound guided repositioning of the dispaced fragments which was performed in all 32 cases. We found a clear postoperative enlargement of canal area (ASP preoperatively 55%, postop. 80%) and midsagittal diameter (MSD preop. 58%, postop. 78%). 10 of 13 patients presented a postoperative improvement of neurological deficit, no neurological deterioration occurred. Fractures with neurological deficit showed more canal compromise (52%) and less midsagittal diameter (MSD compromise 51%) than those without (40% or 39%). There was no correlation between the percentage of spinal canal stenosis and the severity of neurological deficit. Below L 1 the spinal canal is greater than between Th 11 and L 1, so a more important spinal stenosis is tolerated. In case of unstable burst fractures with neurological deficit the ultrasound guided spinal fracture reposition is an effective procedure concerning the necessary improvement of spinal stenosis: an additional ventral approach for the revision of the spinal canal is unneeded. In fractures without neurologic deficit the repositioning of the displaced fragments promises an avoidance of long-term damages such as myelopathia and claudicatio spinalis.

[Magnetic resonance tomography examination of thoracolumbar spinal fractures after fixateur interne stabilization]. / Kernspintomographische Untersuchung thorakolumbaler Wirbelfrakturen nach Fixateur-interne-Stabilisierung.

To analyse the possible injuries of vertebral segments, especially the disc, after unstable thoracolumbar fractures stabilised with AO internal fixator, we performed magnetic resonance imaging (MRI) of the traumatised region after implant removal. There were two aspects of disc degeneration (DD):(1) biochemical changes and (2) structural damage. MRI detects biochemical processes as one aspect of DD that is often small even in the presence of greater structural damage of the nucleus pulposus caused by fracture. None of the patients presented with structural failure of the anulus fibrosus, which is the essential structural component of the vertebral segments with regard to stability. We observed biochemical changes more often in the lower of the two fracture-adjacent discs and alterations of discal shape more often in the upper of the two, whereas loss of height concerned both discs to approximately the same degree. The supporters of upper-disc resection in thoracolumbar fractures justify their procedure among other things with the structural disc damage, such as alteration of shape and loss of height (altogether more frequent in the upper disc). Our observations that a disc with a structurally altered nucleus pulposus can be biochemically intact and can show an intact anulus fibrosus are arguments in favour of disc preservation. With regard to the upper disc, the widespread opinion that complete and regular disc damage requires a resection has to be revised. The question of whether the lower disc should be resected more often because of its greater biochemical changes cannot be answered by the present study alone. Besides the excellent static information in all anatomical structures of the vertebral column available by MRI, a repeat examination in a prone position yields dynamic information on the spinal cord in the case of suspected dorsal adhesions.

[Paget's disease of the proximal ulna--a rare monostotic manifestation]. / Morbus Paget der proximalen Ulna--eine seltene monostotische Manifestation.

Bone changes of the upper extremity are rare manifestations of the M. Paget disease. Most frequently the disease affects the lower extremities, the pelvis followed by the calvarium and others. The rare asymptomatic, monostotic manifestation of Paget's disease of the left proximal ulnae of a 59 year old woman and the way of diagnosis is described. Symptomatic skeletal lesions are detected by radiological examination, bone scintigraphy reveals asymptomatic lesions. Laboratory tests (Alkaline serum phosphatase, Hydroxyproline in urine) monitor the activity of the disease.