[No Blister-Wrapped Pills: Perforation after Ingestion a Blister-Pack]. / Keine Tabletten im Blister: Perforation nach Verschlucken von Tabletten im Blister.

BACKGROUND: Pills in sharp packaging that are accidentally swallowed (blisters) can cause perforations in the gastrointestinal tract, which are only clinically apparent after the emergence of mediastinitis or peritonitis. Mortality is high. PATIENTS: We have seen two cases in cognitively limited patients, one with oesophageal and one with ileal perforation. RESULTS: Despite surgery, the patient with oesophageal perforation died 3 weeks later of multi-organ failure. The patient with ileal perforation survived sepsis after multiple procedures. CONCLUSION: As a consequence, a hospital-wide policy was implemented prohibiting the issue of tablets in blister packaging at the bedside. No more cases have emerged since that time.

[Secondary Splenic Rupture after Initially Inconspicuous CAT Scan]. / Sekundäre Milzruptur bei primär unauffälliger Computertomografie.

BACKGROUND: Splenic injuries occur in 1-5 % of blunt abdominal trauma cases. After initial haemorrhagic compression, secondary delayed spleen rupture can occur with a latency of one day to a month or longer. Mortality is then up to 15 %. The spleen injury is almost always recognisable on CT or ultrasound. CASE HISTORY: In one case from our clinic, secondary splenic rupture occurred in a patient after discharge from hospitalisation, even though the initial CT and ultrasound were unremarkable. The patient survived, and underwent emergent splenectomy 8 days after the trauma. An expert review of the case identified no errors in treatment. CONCLUSION: No case of secondary splenic rupture after initially unremarkable diagnostic studies and clinical course has previously been published. Secondary splenic rupture has a high mortality rate. Patients should be advised of potential complications after hospital discharge, and should return to the hospital immediately in case of symptoms.

[Pericardial perforation 2.5 years after kyphoplasty. A rare complication after cement extravasation]. / Herzperforation 2,5 Jahre nach Kyphoplastie. Eine seltene Komplikation nach Zementaustritt.

Kyphoplasty is an established method in the treatment of osteoporotic spine fractures. In 10-15% of cases cement extravasation and leakage into veins occur. We report about the rare course of an extravasation. In 2008 an osteoporotic compression fracture of L(4) and L(5) in a 62-year-old female patient was treated by kyphoplasty. In the treated vertebra filling of an outgoing vein towards the proximal right side occurred. Postoperatively the patient was free of complaints (VAS preoperative 9/10, postoperative 1/10). In the chest X-ray a small asymptomatic filling of a lung vessel on the left side was present. The patient arrived as an emergency case 2.5 years later with decompensated heart failure. In the chest CT and angiography cement emboli in the lung were seen as well as a perforation of the pericardium with beginning tamponade. A thoracotomy was performed. Intraoperatively two 4 cm long sharp cement pieces were removed from the heart, which had perforated the right ventricle. Leakages were closed by suture. The patient survived the operation and was dismissed after 2 weeks of intensive care for rehabilitation and from there dismissed home. Six months later she had no more problems. When filling vertebra in several levels one must pay attention to introducing cement with a thick consistency, otherwise venous emboli and lung emboli may occur. These are as a rule asymptomatic, but may result in exceptional life-threatening complications.

Comparing telomere length of sister chromatids in human lymphocytes using three-dimensional confocal microscopy.

BACKGROUND: The length of the terminal sequences of linear chromosomes changes dynamically during cellular proliferation. A crucial element in the study of telomere-related regulation mechanisms is the ability to measure telomere lengths of individual chromosomes. Individual telomere lengths can be measured using digital imaging fluorescence microscopy-based techniques. We extended this method using confocal microscopy for the acquisition of three-dimensional (3D) images. Consequently, variations in measured signal intensities due to erroneous focusing are avoided. METHODS: We employed our 3D telomere sizing method to compare telomere lengths of sister chromatids within metaphase preparations from human lymphocytes. The samples were treated following a quantitative fluorescence in situ hybridization (Q-FISH) protocol using fluorescein isothiocyanate (FITC)-labeled telomeric peptidic nucleic acid (PNA) probes and propidium iodide (PI) counterstain. RESULTS: We demonstrated that the telomere lengths of two sister chromatids are not necessarily equal in human lymphocytes. Profound statistical analysis demonstrated significant differences in the distribution of the sister chromatid telomere lengths, but we were not able to prove a discrete distribution of telomere sister ratios. These telomere length differences were more apparent in older individuals. CONCLUSION: Whereas the majority of sister telomere pairs have equal lengths, surprisingly, a minority was significantly different in each individual studied. We are convinced that these observations are not linked to the methodology or the protocol applied. We suggest that a biological phenomenon might be involved.

Monocytic-endothelial cell interaction: regulation of prostanoid synthesis in human coculture.

Coculture of a monocytic cell line (HL-60) and iliacal endothelial cells as an in vitro model of vascular inflammation was investigated for cooperative regulatory mechanisms of prostanoid synthesis under conditions of selective prestimulation. In coculture of endothelial cells and 12-O-tetradecanoylphorbol 13-acetate (TPA)-prestimulated monocytic HL-60 cells the capacity of prostanoid synthesis from arachidonic acid was strongly increased compared with monocultures. Concomitant with up-regulation of specific adhesion molecules, cyclooxygenase (COX) 2 mRNA was induced in endothelial cells in coculture independent of cell contact. HL-60 cells exhibited no alterations in mRNA expression of cyclooxygenases or thromboxane synthase. Coculture of TPA-prestimulated endothelial cells with unstimulated HL-60 cells led to a selectively increased capacity of thromboxane production. Under this condition HL-60 cells up-regulated COX1 and COX2 mRNA, whereas endothelial mRNA levels did not change. Our data demonstrate that the increase in prostanoid synthesis in coculture essentially depends on rapid induction of COX2 mRNA within 2 h.

Prevention of phalloidin-induced lesions on isolated rat hepatocytes by novel synthetic analogues of somatostatin.

Exposure of freshly isolated hepatocytes to phalloidin produced blebs on their surfaces: this phenomenon was time- and dose-dependent and irreversible. When hepatocytes were pretreated with somatostatin or with some of its synthetic analogues, formation of blebs was dramatically reduced. This cytoprotective effect was dose-dependent: the dose-response profiles enabled the determination of the CD50 values, i.e., the concentrations of analogues that yielded 50% cytoprotection. The analogues with sequences of amino acids in the retro form, compared to those in somatostatin-14, exhibited higher cytoprotection; the retro hexapeptide, cyclo(-Phe-Thr-Lys-D-Trp-Phe-D-Pro-), was 27 times more active than somatostatin-14. Specificity of cytoprotection was examined by pretreating hepatocytes with biologically active peptide hormones prior to exposure to phalloidin. On a molar basis, prolactin and thyroid-stimulating hormone possessed activity comparable to that of somatostatin-14, whereas glucagon was twice as active. Insulin, vitamin A and propranolol exercised less than 10% protection. The synthetic analogues of somatostatin are potent protective agents against cell lesions induced by phalloidin. Formation of blebs on hepatocytes by toxins and their prevention by agents of interest may serve as a suitable morphological assay for screening of cytotoxicity and cytoprotection.

Modified somatostatins as inhibitors of a multispecific transport system for bile acids and phallotoxins in isolated hepatocytes.

Somatostatin inhibits the uptake of phallotoxins and of cholic acid in isolated liver cells in a concentration-dependent manner. The inhibition is independent on the preincubation period and fully reversed by switching to a somatostatin-free buffer. Concentrations needed for 50% inhibition decreased 30-80-fold when somatostatin was modified by variation of its amino acid sequence. Some cyclic hexa- or penta-peptides inhibited both kinds of transport more strongly as the original (14 amino acid) somatostatin did. Three of the analogs showed a 2-3-fold higher potency than the others. The most potent compound (cyclo (Phe-Thr-Lys-Trp-Phe-D-Pro) 1 was studied in detail. The IC50 for the initial uptake of phallotoxin (6 microM) or of cholate (6 microM) was 1.5 or 3 microM, respectively. 1 inhibited the uptake of cholate in a competitive manner. The inhibition was independent on the preincubation time, but in contrast to somatostatin not fully reversible after a preincubation of 35 min. Somatostatin as well as its analogs prevented binding of isothiocyanatobenzamido [3H]cholate (an affinity label of the cholate transporter) to isolated plasma membranes from rat liver. The transport inhibition of cholate uptake is unlikely to be a hormonal effect of somatostatin, because the concentrations needed are approx. 1000-fold higher than circulating levels; however, it is apparently possible to increase the inhibitory potency on the tested transport system by modification of the sequence without increase of the well-known hormonal effects (Designing Activity and Receptor-Selectivity in Cyclic Peptide Hormone Analogs, Kessler, H., 18th Ervag Conference, Brussels, 1983).