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11.
Boerhaave’s syndrome: Primary repair vs. esophageal resection—Case reports and meta-analysis of the literature 总被引:3,自引:0,他引:3
Otto Kollmar M.D. Werner Lindemann M.D. Sven Richter M.D. Ingo Steffen M.D. Georg Pistorius M.D. Martin K. Schilling M.D. 《Journal of gastrointestinal surgery》2003,7(6):726-734
Boerhaave’s syndrome is a life-threatening disease with a high mortality. With regard to the heterogeneity of treatment strategies,
no comparative studies exist and recommendations remain controversial. Seventeen cases of Boerhaave’s syndrome operated on
between 1989 and 2000 at our hospital were reviewed retrospectively to compare the time period between perforation and diagnosis,
and the morbidity and mortality among the different treatment options. In addition, we conducted a meta-analysis of the literature
including all series containing five or more patients and compared the findings with our own data. Our patients with a perforation
history of less than 12 hours showed significantly fewer signs of sepsis compared to patients with a history of more than
12 hours. In a comparison of patients with primary repair vs. patients treated with esophageal resection or an exclusion operation,
no differences were found. In the literature, patients with a long period of perforation (more than 24 hours) were treated
more often with an esophageal resection than patients with primary repair. In cases of Boerhaave’s syndrome, primary suturing
of the esophageal perforation should be reserved only for those patients presenting within 12 hours after perforation. In
all other cases, depending on the extent of the tissue damage, a two-stage esophageal resection with cervical esophagostomy
and gastrostomy is recommended as the safest treatment. 相似文献
12.
Martin Døssing Steffen Groth Jørgen Vestbo Ole Lyngenbo 《International archives of occupational and environmental health》1990,62(3):209-212
Summary Among 701 Copenhagen plumbers we examined the lung function of 23 never smokers, who had removed asbestos insulation and intermittently been exposed to high levels of asbestos for about 25 years without being exposed to welding fume. The plumbers had significantly lower TLC, MEF25, MEF50, closing volume and closing capacity in comparison to 23 never smoking electricians without asbestos exposure. There was no reduction in TLCO. Pulmonary clearance of aerosolized 99mTc-DTPA was normal indicating that the asbestos had not induced increases in pulmonary epithelial permeability. However, in 11 of the 23 plumbers the 99m-Tc-DTPA ventilation scintigrams had a slightly irregular and spotty appearance, which together with the results of the lung function tests are suggestive of small airways' dysfunction. None of the subjects had symptoms or clinical signs of lung disease. 相似文献
13.
Steffen Rickes Peter Rauh Daniel Ensberg Christine Uhle und Frank Aedtner 《Medizinische Klinik》2007,102(9):778-780
Ohne Zusammenfassung 相似文献
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The amyloid precursor protein (APP) gives rise to beta-amyloid peptides, which are the main constituents of senile plaques in brains of Alzheimer's disease (AD) patients. The generation of beta-amyloid peptides requires the enzymatic activity of the beta-site APP-cleaving enzyme 1 (BACE1). BACE1 is primarily expressed by neurons and increased BACE1 protein concentrations and enzymatic activities have been reported in the brains of AD patients. However, there is accumulating evidence that, in addition to neurons, reactive astrocytes are capable of expressing BACE1 and, therefore, may contribute to beta-amyloid plaque formation. This suggests that conditions accompanied by chronic astrocyte activation may contribute to developing AD. Non-amyloidogenic processing of the APP can be stimulated by phorbol esters (PEs) and by intracellular diacylglycerol (DAG) generation. This led to the hypothesis that classical and novel protein kinase Cs (PKCs), which are activated by DAG/PEs, regulate APP processing. However, in addition to PKCs, there are other DAG/PE receptors present in neurons which may participate in the modulation of APP processing. Munc13-1, a presynaptic protein with an essential role in synaptic vesicle priming, represents such an alternative target of the DAG second messenger pathway. Using Munc13-1 knock-out mice and human neuroblastoma cells transfected with wild-type and mutant Munc13-1 constructs it was demonstrated that Munc13-1 acts independently of and in parallel with PKC to modulate APP metabolism. Therefore, agonists specific for the Munc13-1 C1-domain or small molecules mimicking the function of the endogenous Munc13-1 activator RIM1 may prove useful to shift APP processing towards the non-amyloidogenic pathway. 相似文献
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To assess the incidence rate and the characteristics of traveler's diarrhea in small children ages 0 to 2 years, children ages 3 to 14 years, and adolescents ages 15 to 20 years a retrospective survey was conducted. Of the pretravel visitors to the Zurich University Vaccination Center, all those ages 0 to 20 years were selected between October, 1987, and May, 1988. They received a questionnaire within 2 weeks after returning home. Of the 446 young travelers who were recruited, 363 (81.3%) could be evaluated. Within 14 days in the tropics or subtropics, traveler's diarrhea occurred in 8 of 20 (40.0%) small children, in 4 of 47 (8.5%) children ages 3 to 6 years, in 10 of 46 (21.7%) children ages 7 to 14 years and in 90 of 250 (36.0%) adolescents (P = 0.0003). In small children the clinical course tended to be severe and prolonged (average duration, 29.5; median, 17.5 days) when compared with other age groups (3 to 5 days). In 40% of all the children the parents reported that they had consistently practiced dietary preventive measures. For self-treatment oral rehydration solutions were used in 5.0% and loperamide in 33.8%. In conclusion adults should be discouraged from taking small children to developing countries unless necessary. Parents should be instructed about how to prevent traveler's diarrhea and about the mainstay of self-therapy in pediatric patients by oral rehydration solutions. 相似文献
19.
Constantly evolving treatment guidelines based on a growing body of randomized controlled trials are helping us to improve outcomes in sepsis. However, it must be borne in mind that proven benefit from individual sepsis treatments does not guarantee synergistic beneficial effects when new treatments are added to sepsis management. Indeed, unexpected harmful interactions are also possible. A good example of this is the conflict between intensive insulin therapy and 'low dose' hydrocortisone in septic shock. The goal of tight glycaemic control is made more complicated by steroid-induced hyperglycaemia. In their recent study, Loisa and coworkers demonstrate a measure that reduces the risk for this interaction. They found continuous infusion of hydrocortisone to be associated with fewer hyperglycaemic episodes and reduced staff workload compared with bolus application. 相似文献
20.
Steffen Roiner Nikolas Bakinde Ulrike Zeitschel Reinhard Schliebs Volker Bigl 《International journal of developmental neuroscience》1998,16(7-8):669-673
The present study was conducted to test the hypothesis that cholinergic basalforebrain neurons are a major source of cerebrospinal fluid (CSF) cholinesterases. To address thisquestion enzyme activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inboth CSF and parietal cortex were assayed following selective lesion of basal forebrain cholinergicneurons by a single intracerebroventricular application of the cholinergic immunotoxin192IgG-saporin. Cholinergic immunolesions led to a dramatic decrease in total AChE activity inparietal cortex, which was due to the specific loss of the G4 molecular form while the activity ofthe G1 form was increased as compared to nonlesioned animals. In contrast, the total enzymeactivity of BChE and its molecular forms were not affected by cholinergic lesion in both parietalcortex and CSF. The data suggest, that cholinergic basal forebrain neurons are seemingly not amajor source of cholinesterases in the CSF, and do not provide any evidence for using CSFcholinesterases as a diagnostic marker of basal forebrain cholinergic cell loss in humans. 相似文献