Weichteilemphysem ungewöhnlichen Ausmaßes

Streptococcus agalactiae, known as a pathogen that causes meningitis and septicemia in neonates, emerges as an invasive organism in nonpregnant adults. This case report describes the fulminant course of a necrotizing fasciitis (NF) with streptococcal toxic shock-like syndrome (STSS) in a 76-year-old diabetic patient caused by S. agalactiae, serotype V. Chronic diseases and immunodeficiency are considered to be risk factors for the acquisition of group B streptococcal disease. Since early surgical treatment in conjunction with antimicrobial and intensive care therapy is critical for the outcome of patients with NF and/or STSS, clinicians should be aware of invasive S. agalactiae infections in adults with subcutaneous emphysema.     

The role of mast cells and histamine in leukocyte-endothelium interactions in four rat strains

 The objective of the present study was to determine the role of mast cells and histamine in leukocyte-endothelium interactions in mesenteric venules of four rat strains: Brown Norway, Lewis, Sprague-Dawley and Wistar. Intravital microscopy showed that the mast cell stabilizer cromoglycate (5 mg/kg i.v. just before exteriorization of the mesentery) did not affect the baseline level and velocity of leukocyte rolling in any of the four strains. This finding is in agreement with the observation that cromoglycate pretreatment only slightly influenced mast cell degranulation in all strains except the Brown Norway. After mast cell stabilization, only in Sprague-Dawley did topical administration of histamine (10^–4 M) result in a significant increase in the level of leukocyte rolling and a decrease in the rolling velocity compared with the time control. Histamine induced leukocyte adhesion only in the Brown Norway strain. In conclusion, the hypothesis presented in other studies, that degranulation of mast cells, and more specifically the release of histamine, is of major importance for the induction of leukocyte-endothelium interactions in rat mesenteric venules is not generally applicable; the present study shows a clear strain dependency. Received: 18 July 1997 / Received after revision: 17 November 1997 / Accepted: 13 March 1998     

Neurobehavioral effects among subjects exposed to high static and gradient magnetic fields from a 1.5 Tesla magnetic resonance imaging system--a case-crossover pilot study.

The interactive use of magnetic resonance imaging (MRI) techniques is increasing in operating theaters. A study was performed on 17 male company volunteers to assess the neurobehavioral effects of exposure to magnetic fields from a 1.5 Tesla MRI system. The subjects' neurobehavioral performances on a neurobehavioral test battery were compared in four 1-hr sessions with and without exposure to magnetic fields, and with and without additional movements. Adverse effects were found for hand coordination (-4%, P < 0.05; Pursuit Aiming II) and near visual contrast sensitivity (-16% and -15%, P < 0.10; Vistech 6000). The results from the remaining tests were inconclusive due to a strong learning effect. No additional effect from gradient fields was detected. The results indicate that working near a 1.5 Tesla MRI system may lead to neurobehavioral effects. Further research is recommended, especially in members of operating teams using interactive MRI systems.     

Peripheral nerve stimulation during MRI: Effects of high gradient amplitudes and switching rates

The application of high gradient amplitudes and switching rates for MRI and spectroscopy, resulting in short rise times for the gradient field and high changes of the magnetic flux density in the patient, is known to possibly evoke peripheral nerve stimulation (PNS) in patients. These effects have been studied on 20 volunteers under different experimental circumstances. The results of these measurements are partially in line with earlier findings reported in the literature. New information is found for the dependence of the PNS threshold level as a function of the rise time of the gradient waveform. The PNS threshold level, expressed in terms of dB/dt, is found to be proportional with t^?05, where t is the switch time for the gradients. Indications are found that |B|, the modulus of the gradient vector field, is more closely related to the PNS threshold level than B_z, the imaging component of the gradient field. From the experiments, it is furthermore concluded that only for the imaging protocols characterized by the application of long bipolar repetitive gradient pulse trains, such as echo-planar imaging, PNS is expected at the reported threshold levels. For the protocols based on spin echo, turbo spin echo, inversion recovery, fast field echo, etc., characterized by shorter gradient pulse trains, the threshold levels are expected to be much higher.     

Epidemic dysentery caused by Shigella dysenteriae type 1: a sentinel site surveillance of antimicrobial resistance patterns in Burundi.

Annual epidemics of bacillary dysentery have been a public health problem in Burundi for the last 14 years. Recent civil unrest, resulting in the displacement of large numbers of people into refugee settlements, has aggravated the situation. We report the results of a nationwide, health-centre based, sentinel site survey to check the drug resistance of Shigella dysenteriae type 1 (Sd1), the causal organism of such epidemics. Shigella spp. (of which 97% were Sd1) were isolated from 73% of the 126 specimens collected from six main sites around the country. There was no difference in culture results from fresh and frozen stool specimens. Overall Sd1 resistance to commonly available antibiotics (sulfamethoxazole + trimethoprim, ampicillin, tetracycline, and chloramphenicol) varied from 77% to 99% and was fairly uniformly distributed over the country. All Sd1 isolates were susceptible to newer drugs, such as ciprofloxacin and ceftriaxone. Resistance to nalidixic acid, the current first line of treatment for bacillary dysentery in Burundi, varied from 8% to 83% in the different sentinel sites; global resistance was 57%.     

A One–Step, Operator–Independent Method for Isolating Islets of Langerhans from the Porcine Pancreas

Abstract: Large–scale isolation of islets of Langerhans is one of the major obstacles in islet transplantation. Until now, isolation methods relied on enzymatic digestion, the duration of which relies on a decision dictated by the operator's experience. This approach has always hindered development of an automated method. The aim of this study was to develop a one–step method based on complete digestion of the pancreas. The original aspect of the technique (derived from the Ricordi method) is use of the University of Wisconsin (UW) solution in the digestion medium and a continuous flow collagenase processing circuit with local cooling and rewarming to allow tissue digestion to proceed at 37°C while settling of the cell suspension takes place at 4°C. A stopcock system permits the alternate use of two settling chambers so that while one is in the circuit, the other can be removed for cen–trifugation, resuspension of the crude islet preparation in collagenase in free UW solution, and further purification in a density gradient system. Ten experiments were performed, and 545, 750 ± 48, 670 purified pig islets were obtained per totally digested pancreas. Histological studies showed cell integrity. Insulin secretion in response to double glucose stimulation under perfusion conditions demonstrated the functional viability of the isolated islets. In conclusion, this one–step method makes it possible to obtain a high number of viable islets of Langerhans in the absence of any decision by an operator, and it should therefore provide basis for an automated method.     

Analysis of a familial three way translocation involving chromosomes 3q, 6q, and 15q by high resolution banding and fluorescent in situ hybridisation (FISH) shows two different unbalanced karyotypes in sibs.

We report on a familial three way translocation involving chromosomes 3, 6, and 15 identified by prometaphase banding and fluorescence in situ hybridisation (FISH). Two mentally retarded sibs with different phenotypic abnormalities, their phenotypically normal sister and mother, and two fetuses of the phenotypically normal sister were analysed. The terminal regions of chromosomes 3q, 6q, and 15q were involved in a reciprocal translocation, in addition to a paracentric inversion of the derivative chromosome 15. Conventional cytogenetic studies with high resolution GTG banding did not resolve this rearrangement. FISH using whole chromosome paints (WCPs) identified the chromosomal regions involved, except the aberrant region of 3q, which was undetectable with these probes. Investigation of this region with the subtelomeric FISH probe D3S1445/D3S1446 showed a balanced karyotype, 46,XX,t(3;15;6) (q29;q26.1;q26), inv der(15) (q15.1q26.1) in two adult females and one fetus. It was unbalanced in two sibs, showing two different types of unbalanced translocation resulting in partial trisomy 3q in combination with partial monosomy 6q in one patient and partial trisomy 15q with partial monosomy 6q in the other patient and one fetus. These represent apparently new chromosomal phenotypes.     

Transmural changes in mast cell density in rat heart after infarct induction in vivo

The cardiac distribution of mast cells was investigated after the induction of acute myocardial infarction in the rat. The left anterior descending coronary artery (LAD) was occluded by ligation in the infarct group, whereas in sham rats only a superficial ligature was placed beside the LAD. Rats of both groups were killed at 4, 7, 14, 21, 35, and 85 days following surgery. Hearts were excised and formalin-fixed. Mast cell densities were monitored in subepicardial and subendocardial layers of the left ventricle (LV) in 6 μm thick toluidine blue-stained cross-sections. In control (non-operated) animals, mast cell densities were comparable in the LV subepicardial and subendocardial layers (1·5–2·0 cells per mm²). Following infarction, the mast cell density at the subepicardial site of the infarction gradually increased, reaching a maximum of 25 cells per mm² on day 21, while a non-significant increase was observed at the subendocardial site. In the non-infarcted regions, the mast cell density increased transiently to reach a maximum of 7 cells per mm² on day 35 in the subepicardial layer. Again, changes in mast cell density in the subendocardial layer were non-significant. In the sham group, a gradual increase to 9 cells per mm² on day 21 and a subsequent decrease to 5 cells per mm² on day 85 were observed in the subepicardial layers. These findings indicate a massive accumulation of mast cells in the subepicardial layers of the infarcted region and a small but significant effect of the surgical procedure on cardiac mast cell deposition, especially in the outer layers of the left ventricle.