[Digital image processing and new media in ENT endoscopy--possibilities and future].
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Biomedical subjects
Publications and source records attributed to H Schmidt.
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OBJECTIVES: We sought to determine the incidence of left atrial (LA) thrombi in patients in sinus rhythm (SR) and with a recent neurologic deficit and to analyze the relation between LA thrombi and LA chamber and appendage function in patients in SR. METHODS: A prospective study was conducted in 869 consecutive patients. The study group consisted of 583 patients in SR (67%). The remaining 286 patients had atrial fibrillation (AF) and served as controls (33%). RESULTS: The incidence of LA thrombi was significantly higher in patients with AF (n = 39 [14%]) compared with patients in SR (n = 6 [1%]; P <.001). Three of 6 patients with thrombi in SR had mitral stenosis, 1 patient had aortic stenosis, 1 patient had coronary artery disease, and another patient had a cardiomyopathy. Of the patients with detected thrombi, those in SR did not receive anticoagulation, whereas those with AF did in 18 cases. Patients with thrombi in SR and with AF did not significantly differ in LA diameter (5.1 +/- 0.8 cm vs 4.8 +/- 0.7 cm; 95% confidence interval [CI], -0.78 to 0.45), left ventricular ejection fraction (46% +/- 13% vs 42% +/- 15%; 95% CI, -18.7 to 7.4), LA appendage area (5.8 +/- 2.7 cm(2) vs 6.7 +/- 3.2 cm(2); 95% CI, -1.9 to 3.6), peak emptying velocity of the LA appendage (0.19 +/- 0.08 m/s vs 0.17 +/- 0.07 m/s; 95% CI, -0.08 to 0.04), or LA spontaneous echo contrast (3. 5 +/- 0.6 vs 3.9 +/- 0.5; 95% CI, -0.06 to 0.45). CONCLUSIONS: LA appendage thrombi are an infrequent cause of thromboembolism in patients in SR and are associated either with mitral valve disease or LA chamber and appendage dysfunction. Routine transesophageal echocardiography for the exclusion of LA thrombi is not recommended in patients in SR without underlying heart disease and normal LA function as assessed by transthoracic echocardiography.
OBJECTIVE: To compare the effectiveness of penicillin V with placebo in the treatment of adult patients with acute maxillary sinusitis in general practice. DESIGN: Randomised, double blind, placebo controlled trial. SETTING: 26 Danish general practices. PATIENTS: 133 adult patients with a clinical diagnosis of acute maxillary sinusitis based on maxillary pain and raised values of either C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR). MAIN OUTCOME MEASURES: Pain score and illness score as well as measurement of CRP and ESR values after initiation of treatment. RESULTS: Penicillin V led to a better recovery than did placebo. The difference was statistically significant 3 days after the initiation of treatment with regard to pain reduction, whereas no significant difference was found with regard to the reduction in the sense of illness. At the end of the study, significantly more patients in the penicillin group were completely free of pain compared to the placebo group. This difference was only found in patients with an initial pain score of more than three. The cure rate was 71% in the penicillin group and 37% in the placebo group. Significantly more patients achieved normal CRP values when treated with penicillin (88%) as opposed to placebo (75%). CONCLUSION: Penicillin V is more effective than placebo in the treatment of acute maxillary sinusitis in adults in general practice, but only in patients with pronounced pain.
UNLABELLED: Severe adenoviral infections such as the necrotizing adenovirus bronchiolitis occur sporadically in infants. Ascertaining the etiologic role of adenovirus in cases of lung disease can pose a diagnostic problem. We present two cases of severe bronchiolitis in previously healthy children in which adenovirus could be shown to be the causing agent. Both children received immunosuppressive therapy with steroids and Cyclosporin for 3 mo and a course of intravenous Ribavirin for 10 d. The results were conflicting: despite therapy Patient 1 died due to respiratory failure, Patient 2 improved notably. CONCLUSIONS: Adenovirus can cause severe bronchiolitis in previously healthy children. Diagnosis may be difficult to achieve. The role of antiviral therapy in the treatment of adenoviral infections remains to be cleared.
UNLABELLED: Cytokine production, neutrophil adhesion to endothelial cells, and release of reactive oxygen species are thought to be critical events in sepsis or ischemia/reperfusion. Modulation of leukocyte responses by anesthetics may have an important role in limiting tissue injury under these conditions. Therefore, we investigated the effect of ketamine on the expression of CD18, CD62L, and oxygen radical production of human neutrophils in vitro and on interleukin-6 production in endotoxin-stimulated human whole blood. Ketamine inhibited both the N-formyl-methionyl-leucyl-phenylalanine- and phorbol 12-myristate 13-acetate-induced up-regulation of CD18 and shedding of CD62L, determined by flow cytometry, in a concentration-dependent manner. Ketamine also caused a significant suppression of oxygen radical generation of isolated human neutrophils. In addition, there was a significant decrease in endotoxin-stimulated interleukin-6 production in human whole blood. The inhibitory effects were similar for racemic ketamine and its isomers S(+)-ketamine and R(-)-ketamine, suggesting that the inhibition of stimulated neutrophil function is most likely not mediated through specific receptor interactions. IMPLICATIONS: Modulation of leukocyte responses by anesthetics may have an important role in limiting tissue injury in sepsis or ischemia/reperfusion. Therefore, we examined the effect of ketamine on stimulated neutrophil functions in vitro. These neutrophil functions were significantly inhibited by ketamine, independent of whether the racemic mixture or isomers were tested.
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OBJECTIVES: To determine the effect of dopexamine, a synthetic catecholamine ligand for dopaminergic and beta2-adrenergic receptors, on intestinal release of adenosine 5'-triphosphate (ATP) degradation products and on intestinal tissue concentrations of high-energy phosphates during endotoxemia. DESIGN: Randomized, controlled trial. SETTING: Experimental laboratory. SUBJECTS: Twenty-one male Wistar rats. INTERVENTIONS: Rats given endotoxin (Escherichia coli lipopolysaccharide [LPS]; 1.5 mg/kg i.v. over 60 mins) were treated with a continuous infusion of dopexamine (DPX; 2.5 microg/kg/min, n = 7, group LPS + DPX) or 0.9% saline (n = 7, group LPS) during a study period of 120 mins. Animals in the control group (n = 7) received a volume-equivalent infusion of 0.9% saline without endotoxin. MEASUREMENTS AND MAIN RESULTS: In all groups, arterial and portal venous concentrations of adenosine, hypoxanthine, and uric acid were measured at baseline and at 60 and 120 mins after the endotoxin challenge, and we calculated the portal venous/arterial concentration differences as an indicator of the intestinal release of the purine compounds. Furthermore, at the end of the study, the intestinal tissue concentrations of the high-energy phosphates ATP, adenosine 5'-diphosphate (ADP), adenosine 5'-monophosphate (AMP), creatine phosphate, and adenosine were determined, and we calculated the adenine nucleotide pool, the ATP/ADP and AMP/adenosine ratios, and the adenylate energy charge of the intestinal tissue. Endotoxemia decreases intestinal tissue ATP, ADP, AMP, and creatine phosphate concentrations, increases tissue adenosine content, and increases the release of hypoxanthine and uric acid from the intestinal tract. Dopexamine attenuates the endotoxin-induced decrease of the intestinal tissue adenine nucleotide pool, the AMP/adenosine ratio, and the release of the ATP-degradation products hypoxanthine and uric acid from the intestinal tract. CONCLUSIONS: Normotensive endotoxemia is associated with a deterioration of the intestinal energy balance and an increased release of ATP degradation products, indicating intestinal tissue ischemia. Furthermore, these results suggest the beneficial effects of dopexamine on pathophysiologic alterations of the intestinal energy metabolism during endotoxemia.
OBJECTIVES: To determine the meaning of leukocyte-endothelial interactions for the development of endotoxin-induced vascular leakage. DESIGN: Randomized, blinded, controlled trial. SETTING: Experimental laboratory. SUBJECTS: Twenty-four male Wistar rats. INTERVENTIONS: After application of fucoidin to prevent leukocyte rolling and adherence (25 mg/kg; n = 8; fucoidin/LPS group) or saline 0.9% (n = 8; LPS group), animals were given an intravenous infusion of endotoxin (Escherichia coli lipopolysaccharide 026:B6; 2 mg/kg/hr) over 120 mins. Animals in the control group (n = 8) received an equivalent volume of saline 0.9%. MEASUREMENTS AND MAIN RESULTS: Leukocyte rolling and leukocyte adherence, red cell velocity, vessel diameters, venular wall shear rate, volumetric blood flow, and macromolecular leakage were determined in mesenteric postcapillary venules using in vivo videomicroscopy at baseline, 60 mins, and 120 mins after start of a continuous endotoxin infusion. Fucoidin prevented leukocyte rolling (baseline, 3+/-2 rollers; 120 mins, 3+/-1 rollers; not significant vs. baseline; p < .01 vs. LPS group) and reduced the adherence of leukocytes at baseline and during endotoxemia and showed only a slight increase in adherent leukocytes (baseline, 100+/-38 cells/mm2; 120 mins, 244+/-68 cells/mm2; p < .05 vs. baseline; p < .01 vs. LPS group). In the LPS group, endotoxin exposure induced a marked increase in adherent leukocytes (baseline, 248+/-24 cells/mm2; 120 mins, 560+/-57 cells/mm2; p < .01). Leukocyte adherence in control animals (control group) did not increase significantly. Macromolecular leakage, expressed as the ratio of perivenular to intravenular fluorescence intensity after injection of fluorescence-labeled albumin, increased from 0.16+/-0.03 to 0.49+/-0.04 (p < .01 vs. baseline; p < .05 vs. control) during the infusion of endotoxin in the LPS group. Fucoidin application did not diminish the extravasation of albumin (baseline, 0.09+/-0.03; 120 mins, 0.61+/-0.10; p < .01 vs. baseline; p < .01 vs. control). CONCLUSIONS: These results demonstrate that despite a significant reduction of adherent leukocytes to the endothelium by fucoidin, there is no reduction in macromolecular leakage, indicating that leukocyte-endothelial interactions only play a minor role for the development of macromolecular leakage and microvascular damage in the early phase of endotoxemia.
Understanding the basic physics of sound penetration into ocean sediments is essential for the design of sonar systems that can detect, localize, classify, and identify buried objects. In this regard the sound speed of the sediment is a crucial parameter as the ratio of sound speed at the water-sediment interface determines the critical angle. Sediment sound speed is typically measured from core samples using high frequency (100's of kHz) pulsed travel time measurements. Earlier experimental work on subcritical penetration into sandy sediments has suggested that the effective sound speed in the 2-20 kHz range is significantly lower than the core measurement results. Simulations using Biot theory for propagation in porous media confirmed that sandy sediments may be highly dispersive in the range 1-100 kHz for the type of sand in which the experiments were performed. Here it is shown that a direct and robust estimate of the critical angle, and therefore the sediment sound speed, at the lower frequencies can be achieved by analyzing the grazing angle dependence of the phase delays observed on a buried array. A parametric source with secondary frequencies in the 2-16 kHz range was directed toward a sandy bottom similar to the one investigated in the earlier study. An array of 14 hydrophones was used to measure penetrated field. The critical angle was estimated by analyzing the variations of signal arrival times versus frequency, burial depth, and grazing angle. Matching the results with classical transmission theory yielded a sound speed estimate in the sand of 1626 m/s in the frequency range 2-5 kHz, again significantly lower the 1720 m/s estimated from the cores at 200 kHz. However, as described here, this dispersion is consistent with the predictions of the Biot theory for this type of sand.
In situ measurements of scattering strength are often obtained by analyzing the early-time, high-angle reverberation from bottom and subbottom features. In order to provide insight into the mechanisms which cause bottom reverberation, and to their distinguishing characteristics, it is necessary to have a capability for modeling both the rough surface and the volume scattering mechanisms. For high-angle, early-time backscatter, the most appropriate approach is to use a spectral integral representation, which naturally includes the continuous spectrum important for this angular regime. A rough surface scattering theory developed earlier in this framework has provided important insights into wave scattering and penetration physics at the seafloor. Here a consistent representation for the subbottom scattering is developed and examples are provided which illustrate the observable differences between the two scattering mechanisms.
This paper presents preliminary results of a recent study whose overall objectives are to determine the mechanisms contributing significantly to subcritical acoustic penetration into ocean sediments, and to quantify the results for use in sonar performance prediction for the detection of buried objects. In situ acoustic measurements were performed on a sandy bottom whose geoacoustical and geomorphological properties were also measured. A parametric array mounted on a tower moving on a rail was used to insonify hydrophones located above and below the sediment interface. Data covering grazing angles both above and below the nominal critical angle and in the frequency range 2-15 kHz were acquired and processed. The results are compared to two models that account for scattering of sound at the rough water-sediment interface into the sediment. Although all possible mechanisms for subcritical penetration are not modeled, the levels predicted by both models are consistent with the levels observed in the experimental data. For the specific seafloor and experimental conditions examined, the analysis suggests that for frequencies below 5-7 kHz sound penetration into the sediment at subcritical insonification is dominated by the evanescent field, while scattering due to surface roughness is the dominant mechanism at higher frequencies.
An energy-conserving spectral solution is derived and tested. A range-dependent medium is approximated by a sequence of range-independent regions. In each region, the acoustic field is represented in terms of the horizontal wave-number spectrum. A condition corresponding to energy conservation is derived for the vertical interfaces between regions. The accuracy of the approach is demonstrated for problems involving sloping ocean bottoms. The energy-conserving spectral solution is less efficient than the energy-conserving parabolic equation solution, but might be suitable for generalization to problems involving elastic bottoms.
We have isolated Shiga toxin (Stx)-producing Escherichia coli (STEC) strains from the feces of feral pigeons which contained a new Stx2 variant gene designated stx(2f). This gene is most similar to sltIIva of patient E. coli O128:B12 isolate H.I.8. Stx2f reacted only weakly with commercial immunoassays. The prevalence of STEC organisms carrying the stx(2f) gene in pigeon droppings was 12.5%. The occurrence of a new Stx2 variant in STEC from pigeons enlarges the pool of Stx2 variants and raises the question whether horizontal gene transfer to E. coli pathogenic to humans may occur.
Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) produce the characteristic "attaching and effacing" (A/E) lesion of the brush border. Intimin, an outer membrane protein encoded by eae, is responsible for the tight association of both pathogens with the host cell. Several eae have been cloned from different EPEC and EHEC strains isolated from humans and animals. These sequences are conserved in the N-terminal region but highly variable in the last C-terminal 280 amino acids (aa), where the cell binding activity is localized. Based on these considerations, we developed a panel of specific primers to investigate the eae heterogeneity of the variable 3' region by using PCR amplification. We then investigated the distribution of the known intimin types in a large collection of EPEC and EHEC strains isolated from humans and different animal species. The existence of a yet-unknown family of intimin was suspected because several EHEC strains, isolated from human and cattle, did not react with any of the specific primer pairs, although these strains were eae positive when primers amplifying the conserved 5' end were used. We then cloned and sequenced the eae present in one of these strains (EHEC of serotype O103:H2) and subsequently designed a PCR primer that recognizes in a specific manner the variable 3' region of this new intimin type. This intimin, referred to as "epsilon," was present in human and bovine EHEC strains of serogroups O8, O11, O45, O103, O121, and O165. Intimin epsilon is the largest intimin cloned to date (948 aa) and shares the greatest overall sequence identity with intimin beta, although analysis of the last C-terminal 280 aa suggests a greater similarity with intimins alpha and gamma.
An infectious Shiga toxin (Stx) 2e-converting bacteriophage (phiP27) was isolated from Stx2e-producing Escherichia coli ONT:H(-) isolate 2771/97 originating from a patient with diarrhea. The phage could be transduced to E. coli laboratory strain DH5alpha, and we could show that lysogens were able to produce biologically active toxin in a recA-dependent manner. By DNA sequence analysis of a 6,388-bp HindIII restriction fragment of phiP27, we demonstrated that the stx(2e) gene was located directly downstream of ileZ and argO tRNA genes. Although no analogue of an antiterminator Q encoding gene was present on this fragment, a lysis cassette comprising two holin genes which are related to the holin genes of Pseudomonas aeruginosa phage phiCTX and a gene homologous to the endolysin gene gp19 of phage PS3 were detected. The results of our study demonstrated for the first time that Stx2e can be encoded in the genome of an infectious bacteriophage.
The stx-flanking regions of 49 Shiga toxin-producing Escherichia coli strains and nine Shigella dysenteriae serotype 1 strains containing either stx, stx(1), stx(2), or stx(2) variant genes, were examined. We analyzed these regions by PCR using a set of primers with one primer specific for the respective stx gene and a second primer complementary to sequences of Stx phages H-19B and 933W. We further characterized the amplification products by restriction endonuclease digestion and nucleotide sequencing. PCR products of stx(1)-containing E. coli strains of serogroups O157, O26, and 0103 showed the same lengths and similar restriction patterns. However, we failed to amplify the 3' stx-flanking region in stx(1)-harboring E. coli O111:H(-) strains. Stx2-producing E. coli strains revealed amplification products of different lengths and restriction patterns, suggesting greater heterogeneity than in stx(1)-positive strains. We also obtained specific PCR products for two Stx2c-producing and seven Stx2f-producing E. coli strains when they were subjected to PCR analysis. In nine S. dysenteriae type 1 strains, H-19B- and 933W-specific primers amplified only the 3' stx-flanking region. The results of our study demonstrate that the stx genes of all strains investigated are continuous with phage sequences. Whereas almost all strains except E. coli O111:H(-) strains were associated with a S-like gene, association with Q could not be demonstrated in nine S. dysenteriae type 1 strains and three E. coli strains. Furthermore, we showed that the organization of the stx-flanking regions is similar in all strains investigated, whereas fine-structure analysis showed subtle differences among the sequences examined. Our results support the hypothesis that stx genes in E. coli and S. dysenteriae are generally phage-borne.
Fifty-five Shiga toxin (Stx)-producing Escherichia coli (STEC) O26:H11 and O26:H(-) strains isolated from humans between 1965 and 1999 in Germany and the Czech Republic were investigated for their chromosomal and plasmid characteristics. All motile (n = 23) and nonmotile (n = 32) STEC O26 strains were shown to possess the identical flagellin subunit-encoding gene (fliC). We observed a striking recent shift of the stx genotype from stx(1) to stx(2) among the STEC O26 isolates. While stx(1) was the exclusive genotype identified in our collection until 1994, 94% of the isolates obtained after 1997 possessed stx(2) either alone (71%) or together with stx(1) (23%). Plasmid profiling demonstrated a remarkable heterogeneity with respect to plasmid sizes and combinations. Southern blot analysis of plasmid DNA with probes specific to potential accessory virulence genes revealed considerable additional variability in gene composition and arrangement. Pulsed-field gel electrophoresis (PFGE) differentiated 16 subgroups among the 55 STEC O26 strains. Using these techniques we demonstrate the emergence of a new clonal subgroup characterized by PFGE pattern A and a unique combination of virulence markers including stx(2) and a single, approximately 90-kb plasmid harboring the enterhemorrhagic E. coli hlyA and etp genes. The proportion of PFGE subgroup A strains among STEC O26 isolates rose from 30% in 1996 to more than 50% in 1999. Four clusters of infections with the clonal subgroup A were identified. We conclude that the STEC serogroup O26 is diverse and that pathogenic clonal subgroups can rapidly emerge during short intervals. The extensive genetic diversity of STEC O26 provides a basis for molecular subtyping of this important non-O157 STEC serogroup.
Fifty-seven Escherichia coli O26 strains isolated from patients in six countries were investigated by PCR restriction fragment length polymorphism (RFLP) analysis of the flagellin-encoding (fliC) gene (fliC RFLP analysis). The strains were determined by serotyping to belong to five different H types or were nonmotile. The fliC RFLP analysis revealed only two different patterns among the 57 strains. One fliC RFLP pattern was displayed by 54 strains and was identical to that of E. coli H11 reference strain Su4321-41. The other fliC RFLP pattern was observed for three strains and was identical to that for E. coli H32 reference strain K10. The 54 strains with the H11 fliC RFLP pattern included 22 strains of serotype O26:H11, 23 nonmotile strains, and 9 strains that were initially serotyped as H2, H8, H21, and H32 but that were confirmed to express H11 by repeat serotyping. All 54 strains with the H11 fliC RFLP pattern contained the attaching-and-effacing (eae) gene. The three strains with the H32 fliC RFLP pattern belonged to serotype O26:H32, and all were eae negative. The fliC genes of 14 selected E. coli O26:H11 strains isolated between 1964 and 1999 had identical nucleotide sequences. Our results demonstrate that E. coli O26 strains that carry the eae gene belong exclusively to the H11 clonal complex. Since there were no H11 fliC allelic variations among the O26 strains tested, E. coli O26:H11 may have emerged recently. The fliC PCR-RFLP test is a reliable, easy-to-perform, and rapid method for determination of the H types of E. coli O26 isolates.