[The diagnostic value of thoracic computerized tomography in severe thoracic trauma].
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Adolescent↗
Biomedical subjects
R Hoffmann
Publications and source records attributed to R Hoffmann.
[Combination of the Ilizarov ring fixator with the unilateral AO tube fixator. Initial clinical experiences with the hybrid system].
Ring fixation of the tibia is difficult because of soft tissue transfixation and the size and weight of the external fixator. To increase the patients comfort K-wire and half-pin fixation are combined in a new hybrid configuration. The Ilizarov ring fixator with K-wire or Schanz screw fixation is combined with the unilateral AO fixator. This configuration has so far been used in 17 cases: in the proximal and intraarticular tibia in 7 cases, in the distal tibia in 8 cases and in the femur in 2 cases. As experience with the hybrid system widens indications accepted are metaphyseal and intraarticular fractures of the tibia with severe soft tissue damage, open fractures, segmental defects and fractures of the tibia that cannot be nailed. Loosening of the hybrid construction requiring an additional operative procedure has not occurred. The hybrid system is minimally invasive and allows early weight-bearing. It has the advantages of less transfixation of the soft tissue, an easy operative technique and more comfort with higher patient compliance, and the options for corrective procedures are the same as with the conventional Ilizarov technique. Our preliminary first experience with this system is encouraging; it is especially useful for problematic epi- and metaphyseal fractures with severe soft tissue damage.
Adult↗
The new unreamed AO nails for the tibia and the femur.
The advantages of the unreamed nailing technique compared to the reamed procedure are less damage to bone vascularity, lower intramedullary pressure during the operation and a fast operation time. These new solid nails with high mechanical stiffness and no central dead space have extended the nail indications for tibial as well as for femoral fractures, particularly in tibial shaft fractures with severe soft tissue damage and in polytraumatized patients with a femoral shaft fracture. Besides these advantages the new AO unreamed femur nail has a modular proximal interlocking system, which increases significantly the range of indications for nailing. Not only very high subtrochanteric femur fractures can be stabilized with greater stability, but also combined ipsilateral fractures of the shaft and the proximal femur can be treated with this new nail. The first clinical results of the AO unreamed nails for the tibia as well as for the femur are very encouraging. The unreamed nails prove to be excellent implants in the treatment of long bone fractures of the lower extremity.
Adult↗
[Surveillance of patients with chronic inflammatory intestinal diseases: problems relevant to clinical practice].
For control of activity of inflammatory bowel diseases, clinical signs and acute-phase proteins are of higher value compared to endoscopy; however this method is necessary for supervision of patients with ulcerative colitis for detection of malignancies. In patients with longstanding and extensive ulcerative colitis, a consequent supervision permits to prevent cancer development markedly. New aminosalicylates are effective in preventing relapse in ulcerative colitis and perhaps in Crohn's disease. Deficiency in vitamins and minerals has to be recognized and balanced. Patients suffering from Crohn's disease should quit smoking because nicotine is worsening the course of the disease.
Colitis, Ulcerative↗
[Antibiotic prophylaxis in diagnostic and therapeutic endoscopic procedures].
Antibiotic prophylaxis is recommended for patients at risk for developing bacterial endocarditis as a sequel of bacteremia during endoscopy. In addition antibiotics are necessary for endoscopic procedures with a high risk of infection such as endoscopic retrograde cholangio-pancreatography in patients with stenosis of the bile or pancreatic duct and percutaneous endoscopic gastrostomy.
Anti-Bacterial Agents↗
Tissue specificity of rat mitochondrial dimethylglycine dehydrogenase expression.
Expression of mitochondrial dimethylglycine dehydrogenase (Me2GlyDH) was analysed in various tissues, liver cell types and developmental stages of the rat. Total RNA extracted from liver, spleen, brain, kidney, lung and heart was reverse-transcribed into cDNA and amplified with Me2GlyDH cDNA-specific oligonucleotides by PCR. Expression of the enzyme was observed mainly in liver and kidney. In addition, Me2GlyDH mRNA could be demonstrated in total RNA samples of lung, heart and brain but was barely detectable in spleen total RNA. In RNA prepared from 14-day rat embryos, Me2GlyDH-specific mRNA was clearly present. Among various liver cell types, besides hepatocytes, endothelial cells showed a high level of Me2GlyDH mRNA expression. There was no amplification product detectable in liver macrophages (Kupffer cells) and only a very faint one in fat-storing cells (Ito cells). Western blots confirmed at the protein level the predominant expression of the enzyme in liver and kidney, but Me2GlyDH protein was also present in the protein extract of lung, heart, spleen and brain. Immunohistochemical staining of liver slices with Me2GlyDH-specific antiserum revealed that expression of this enzyme is evenly distributed throughout the liver tissue. In the kidney, expression of the enzyme was located in the proximal tubule cells. Our results demonstrate that, contrary to the previously assumed liver-restricted expression, this enzyme is specifically expressed predominantly in the liver and kidney, but, in addition, it is detectable in many other tissues of the rat.
Aging↗
The Saccharomyces cerevisiae gene PPH3 encodes a protein phosphatase with properties different from PPX, PP1 and PP2A.
A clone encoding the catalytic subunit of a protein phosphatase from Saccharomyces cerevisiae was isolated. Except for replacement of IIe-245 by Met the structure of the phosphatase was identical to that encoded by PPH3 (Ronne, H., Carlberg, M., Hu, G. Z. and Nehlin, J. O. (1991). Mol. Cell. Biochem. 11, 4876-4884) and exhibited 63% sequence identity to PPX cloned from a rabbit liver cDNA library (Brewis, N.D., Street, A.J., Prescott, A.R. and Cohen, P.T.W. (1993). EMBO J. 12, 987-996). Expression of active enzyme was achieved in Escherichia coli mutants which were generated by a genetic selection based on functional complementation of bacterial phosphoserine phosphatase. Though some of the properties of PPH3 resembled those of protein phosphatase 2A and PPX, others were different. PPH3 exhibited lower sensitivity against inhibition by okadaic acid, showed different substrate specificity and required a divalent cation (Mn2+ was preferred before Mg2+ and Ca2+) for activity when assayed with phospho-histone as a substrate. However, 25% of maximum activity was observed in the absence of divalent cations when the peptide LRRAS(P)LG was used as substrate. The PPH3-protein was also identified by chromatography of extracts from S. cerevisiae on DEAE-cellulose. Protein immunoreactive with an antiserum raised against the non-conserved N-terminal 53 amino acids of PPH3 was coeluted with a single peak of LRRAS(P)LG dephosphorylating activity.
Amino Acid Sequence↗
Regulation of the mRNA expression for tumor necrosis factor-alpha in rat liver macrophages.
Kupffer cells are known to produce tumor necrosis factor-alpha upon stimulation with endotoxin or viruses. This tumor necrosis factor-alpha synthesis is suppressed by prostaglandin E2 or dexamethasone. Using Northern blotting and reverse transcriptase-polymerase chain reaction, it is demonstrated that endotoxin-induced tumor necrosis factor-alpha synthesis is blocked by prostaglandin E2 or dibutyryl 3':5'-cyclic adenosine monophosphate on the transcriptional level. Tumor necrosis factor-alpha itself suppressed endotoxin-evoked tumor necrosis factor-alpha mRNA expression when given in a narrow time interval with lipopolysaccharide. Interleukin-10 of human or mouse origin also inhibited the synthesis of tumor necrosis factor-alpha mRNA and protein when given more than 2 h prior to the endotoxin challenge. The suppressive effect of prostaglandin E2 lasted for more than 36 h while IL-10 blocked tumor necrosis factor-alpha production for barely 24 h. Dexamethasone reduced the endotoxin-induced tumor necrosis factor-alpha mRNA formation by approximately 50% only, although it led to nearly complete inhibition of the synthesis of the mature protein. Taken together with reverse transcriptase-polymerase chain reaction data revealing significant amounts of tumor necrosis factor-alpha mRNA in resting Kupffer cells, an additional posttranscriptional regulation of tumor necrosis factor-alpha synthesis has to be assumed. Tumor necrosis factor-alpha mRNA was not induced by interferon-gamma, interleukin-1 beta or interleukin-6 (the latter two cytokines are also synthesized by Kupffer cells), but a 24-h prestimulation of liver macrophages with interferon-gamma or phorbol ester had a modest priming effect.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Regulation of tumor necrosis factor-alpha-mRNA synthesis and distribution of tumor necrosis factor-alpha-mRNA synthesizing cells in rat liver during experimental endotoxemia.
Stimulated liver macrophages (Kupffer cells) are known to release a variety of inflammation-related substances, e.g. cytokines, prostanoids, and reactive oxygen intermediates. For instance, exposure of Kupffer cells in vitro to lipopolysaccharide (endotoxin) leads to a strongly enhanced synthesis of the mRNA for tumor necrosis factor-alpha, the release of the mature protein into culture media. These events are influenced by prostanoids and corticoid hormones. Kupffer cells are thought to be the only source of tumor necrosis factor-alpha within the hepatic sinusoid, but neither this cell specificity nor the regulatory influence of glucocorticoids or prostanoids has been confirmed in the intact organ. Using non-radioactive in situ hybridization, it was possible to obtain specific signals for tumor necrosis factor-alpha-mRNA in individual Kupffer cells uniformly distributed (as compared to Kupffer cells detected by immunohistochemistry) throughout the liver. Kupffer cells were the only cells in the hepatic sinusoids of lipopolysaccharide-perfused livers to express mRNA for tumor necrosis factor-alpha. Simultaneous addition of endotoxin plus dexamethasone and endotoxin and prostaglandin E2 completely suppressed the synthesis of this mRNA. Unexpectedly, the presence of mRNA for tumor necrosis factor-alpha was also detected in the intrahepatic bile duct epithelium of lipopolysaccharide-perfused livers. It is known that biologically active endotoxin is secreted via the bile ducts. These results seem to indicate that bile duct epithelium responds to inflammatory agents with synthesis of tumor necrosis factor-alpha-mRNA. One must also consider new functional aspects of bile duct epithelium in chronic inflammatory diseases, e.g. primary biliary cirrhosis, chronic sclerosing cholangitis or graft-versus-host disease.
Animals↗
Regulation of interleukin-6 receptor expression in rat Kupffer cells: modulation by cytokines, dexamethasone and prostaglandin E2.
Interleukin-6 has a variety of biological effects, mainly on the immune system. The regulation of this signal at both the site of production and the site of action is necessary to maintain the organism's homeostasis. In the microenvironment of the hepatic sinusoids, Kupffer cells as resident macrophages are the most potent source of interleukin-6 during inflammation. This cytokine is an important signal to hepatocytes during the early stages of the acute-phase response, leading to the expression of several major plasma proteins. Kupffer cells were found to express interleukin-6 receptor constitutively. Interleukin-6 decreased the level of interleukin-6 receptor mRNA, indicating an autocrine pathway by which Kupffer cells regulate their responsiveness to interleukin-6. Furthermore, lipopolysaccharide, tumor necrosis factor-alpha, interferon-gamma, interleukin-1 beta and phorbol ester induced interleukin-6 production and, at the same time, suppressed the level of interleukin-6 receptor mRNA. The existence of an autocrine loop in rat Kupffer cells may be physiologically relevant, as it would contribute to a regulated interleukin-6 signal chain in the liver. The anti-inflammatory mediators dexamethasone or PGE2 and its second messenger, cyclic AMP, increased interleukin-6 receptor mRNA, whereas prostaglandin D2 or the Ca2+ ionophore, A 23187, were without effect. The changes in interleukin-6 mRNA were paralleled by the number of interleukin-6 receptors present on Kupffer cells as detected by binding of 125I-interleukin-6. These results suggest the existence of control mechanisms involving several soluble mediators that help balance the level of interleukin-6-R mRNA in rat liver macrophages.
Animals↗
Staphylococcal scalded skin syndrome (SSSS) and consecutive septicaemia in a preterm infant.
Staphylococcal scaled-skin syndrome (SSSS) is a toxin-related epidermolytic disease that usually affects infants and children under 5 years. We report herein a case of a premature infant who had developed SSSS after an infection of the pharynx with staphylococci and who died of septicaemia due to pseudomonas aeruginosa. The primary mechanism of action of epidermolysin still remains unknown. We demonstrate that acantholysis is due to an early edema of the intercellular space with separation of ultrastructurally unaltered desmosomes.
Humans↗
[Improved diagnosis of stress fractures with contrast MRI].
MRI is of growing importance for diagnosing bone pathology. Application of additional gadolinium-DTPA contrast medium allows safe differentiation of stress fractures from pathological fractures due to the characteristic perifocal contrast enhancement in the T1 sequences. This phenomenon is exemplified by a case report of a stress fracture of the femoral neck in a long-distance runner.
Adult↗
[Intestinal strongyloidiasis and isosporiasis in AIDS].
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Acquired Immunodeficiency Syndrome↗
Transoesophageal pacing echocardiography for detection of restenosis after percutaneous transluminal coronary angioplasty.
Non-invasive documentation of restenosis after successful percutaneous transluminal coronary angioplasty (PTCA) remains a problem. Thus, transoesophageal pacing echocardiography (TPE) with simultaneous rapid atrial pacing via the same probe, a recently validated method for detection of coronary artery disease, was used in 60 patients for detection of restenosis after successful PTCA (54 patients with one and six patients with multivessel PTCA). The patients came for routine follow-up angiography 5.4 +/- 3.7 months after PTCA regardless of clinical status. Restenosis (diameter stenosis > or = 50%) was demonstrated in 22 patients. Disease progression in previously normal vessels was noted in three additional patients. Results for detection of restenosis and disease progression were compared to exercise ECG and in 40 patients to Tc-99m methoxy-isobutyl-isonitrile (MIBI)-radionuclide perfusion imaging. Diagnostic standard exercise ECG could be performed in only 38 patients, due to peripheral vascular disease, joint disease or premature exhaustion in the rest of patients. TPE was non-diagnostic in two patients due to ineffective pacing or patient discomfort. Sensitivity of TPE for detection of restenosis and disease progression after PTCA was 84% compared with 50% and 86% for exercise ECG and Tc-99m MIBI-SPECT (P < 0.03 and ns), respectively. Specificity of TPE (85%) was also higher than that of exercise ECG (59%, P < 0.03) and comparable to the specificity of MIBI-SPECT (84%). Overall accuracy of TPE was far superior to exercise ECG and similar to MIBI-SPECT (84% vs 54% and 85%) (P = 0.0007 and ns, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Angioplasty, Balloon, Coronary↗
Altered left ventricular diastolic function post-atrial pacing in coronary artery disease and left ventricular hypertrophy: further insights by pulmonary venous flow analysis.
Left ventricular filling dynamics during acute pacing-induced myocardial ischaemia were assessed using transoesophageal atrial pacing and simultaneous Doppler measurements of pulmonary venous and mitral flow. All patients (10 with CAD and 12 with left ventricular hypertrophy due to hypertrophic cardiomyopathy; HCM) were in sinus rhythm and patients with mitral insufficiency were excluded. Data were compared with those of a control group (n = 10). Measurements were obtained at baseline (heart rate 84 +/- 14 beats.min-1) and immediately after atrial pacing via the same transoesophageal echocardiography (TEE) probe after stepwise increase of the pacing rate to 133 +/- 12 beats.min-1. Heart rate immediately after pacing was 83 +/- 13 beats.min-1. Time velocity integrals (TVI) were calculated at baseline and after pacing for the following flows: early (E) and late (A) mitral flows, as well as antegrade systolic (S), diastolic (D) and retrograde diastolic (R) pulmonary venous flows. In the control group none of the flow parameters changed significantly after pacing compared with baseline data. In contrast, in CAD patients, the TVI of the E wave, the TVI E/A ratio as well as the pulmonary venous flow changed significantly after pacing (7.3 to 5.5 cm, P < 0.05, 1.7 to 1.1, P < 0.01 and 1.0 to 2.1 cm, P < 0.001, respectively). HCM patients also showed significant changes: TVI E/A ratio post-pacing decreased from 1.9 to 1.4 (P < 0.05), and the pulmonary venous reverse flow integral increased from 1.3 to 2.8 cm (P < 0.0001). Analysis of variance showed the TVI E/A ratio to be significantly dependent on pacing (P = 0.012). The pulmonary venous retrograde flow was found to be influenced by the presence of disease (P = 0.033 before and P = 0.0001 after pacing) and in all cases by pacing (before vs after pacing; P = 0.0001). Pacing resulted in significantly different changes in the TVI E/A ratio and the TVI of the retrograde pulmonary venous flow for CAD and HCM patients compared with those of control subjects. In patients with CAD and HCM, rapid atrial pacing results in a decreased early to late ventricular filling ratio because of impaired relaxation, despite presumably increased filling pressure. Retrograde pulmonary venous flow increased because of increased filling pressure and operating left ventricular stiffness.
Adult↗
Cytokine mRNA levels in Alopecia areata before and after treatment with the contact allergen diphenylcyclopropenone.
Although the nature of the noxious signal and the anatomical target in alopecia areata (AA) are still unknown, it has been assumed that CD4+ T lymphocytes surrounding and infiltrating the hair bulb might trigger the hair loss. As these T lymphocytes do not promote cytotoxic activity we hypothesize that AA is triggered by cytokines. Topical immunotherapy with diphenylcyclopropenone (DCP) is at present the most effective approach. If it is true that AA results from a distinct cytokine pattern, we can hypothesize that the beneficial effect of DCP should be mediated by locally secreted cytokines during the contact allergy. Using semiquantitative reverse transcription-polymerase chain reaction with RNA extracted from scalp biopsies from patients with AA before and after successful treatment with DCP, and from healthy controls we detected a T-cell response with increased steady state mRNA levels for interferon (IFN)-gamma, interleukin (IL)-1 beta, and IL-2 in untreated AA of the totalis type. After DCP treatment, the IFN-gamma expression was reduced but still above the constitutive level found in controls, whereas mRNA expression of IL-2, IL-8, IL-10, and tumor necrosis factor-alpha was increased. Our results point towards cytokines involved in the pathogenesis in AA. A TH1 type cytokine pattern is present in untreated AA, and this is modified by cytokines secreted during DCP treatment. IL-10 has recently been described as an immunomodulator of the TH1 response and, therefore, we hypothesize that basal keratinocytes or lesional T cells secrete bioactive IL-10 after DCP application, resulting in an inhibitory effect on lesional T lymphocytes. This hypothesis would explain the effectiveness of DCP and implies the theoretical possibility of a response to topical or intralesional application of recombinant IL-10.
Adult↗
1H and 31P NMR spectroscopy of phosphorylated model peptides.
The model peptides glycylglycyltyrosylalanine (Gly-Gly-Tyr-Ala), glycylglycylthreonylalanine (Gly-Gly-Thr-Ala) and glycylglycylserylalanine (Gly-Gly-Ser-Ala) were phosphorylated at the hydroxyl groups of their tyrosyl, threonyl and seryl residues, respectively, and characterized by 31P and 1H NMR spectroscopy. The pKa-value of the phosphoryl group in the tyrosine-containing peptide determined from the pH dependence of chemical shifts is 5.9, the 31P chemical shifts at low pH (4.0) and high pH (8.0) are -3.8 and 0.2 ppm, respectively. Phosphorylation also leads to significant shifts of the 1H NMR resonances of the tyrosine residue; the amide resonance is shifted -0.02 ppm, the H alpha resonance 0.06 ppm, the H beta resonances 0.10 and -0.04 ppm, the H delta resonances 0.02 ppm and the H epsilon resonances 0.26 ppm. The pKa-value of the phosphoryl group in the threonine peptide determined from the pH dependence of chemical shifts is 6.1; the 31P chemical shifts at low pH (4.0) and high pH (8.0) are -0.1 and 4.8 ppm, respectively. The corresponding values for the serine peptide are 6.1 (pKa), 0.6 ppm and 4.9 ppm. Phosphorylation also leads to significant shifts of the 1H NMR resonances of the threonine and serine residues. In the threonine residue the amide resonance is shifted 0.25 ppm, the H alpha-resonance -0.43 ppm, the H beta-resonance 0.03 ppm and the H gamma-resonance 0.09 ppm. In the serine residue the amide resonance is shifted 0.21 ppm, the H alpha-resonance -0.17 ppm, and the H beta-resonances 0.17 ppm.
Amino Acid Sequence↗
Rat liver macrophages express the 55 kDa tumor necrosis factor receptor: modulation by interferon-gamma, lipopolysaccharide and tumor necrosis factor-alpha.
Tumor necrosis factor-alpha is an important mediator of various inflammatory and immune responses. Its biological action is crucially dependent on interaction with specific cell surface receptors. Two different receptors for TNF-alpha with molecular masses of 55 and 75 kDa have been described. Here, the presence of a 55 kDa TNF receptor mRNA and the expression of its protein is demonstrated in rat liver Kupffer cells. TNF-alpha receptor was purified from detergent-solubilized rat Kupffer cells by adsorption to recombinant human TNF-alpha-Sepharose. One band of approx. 55 kDa was seen in SDS PAGE. An antibody raised against the 55 kDa TNF receptor bound specifically to the purified receptor as revealed by immunoblot analysis. Using Northern blotting, neither LPS nor TNF-alpha altered the expression of 55 kDa TNF-R mRNA, although the exposure of Kupffer cells to LPS decreased the binding of 125I-labelled TNF-alpha. Interferon-gamma clearly enhanced the level of 55 kDa TNF-R mRNA; this effect was abolished by transcriptional but not by translational inhibitors. The increase in 55 kDa TNF-R mRNA was maximal at 2-4 h of exposure of IFN-gamma. This cytokine also increased the binding of 125I-TNF-alpha to Kupffer cells. On the other hand, the amount of 55 kDa TNF-R transcripts was reduced after treatment with dexamethasone. These data suggest that in Kupffer cells the expression of the 55 kDa TNF-R is regulated at the transcriptional level.
Animals↗