[Indirect MR-arthrography: optimized method and initial clinical experiences in early degenerative damage of the ankle joint].
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Biomedical subjects
Publications and source records attributed to T Sommer.
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PURPOSE: To evaluate the range of normal contrast enhancement behaviour in dynamic MR mammography of healthy breast parenchyma, and to reduce false-positive results caused by incidental contrast enhancing lesions. MATERIALS AND METHODS: We performed a prospective two-armed study on 20 healthy premenopausal volunteers who were examined four times within one month (Group 1) or during four consecutive months (Group 2). Incidence, prevalence, morphology, and contrast enhancement pattern of lesions were evaluated. RESULTS: 82% (9/11 of Group 1) and 78% (7/9 of Group 2) showed at least one of a total of 60 contrast enhancing lesions. In 54% or 33% (Group 1 or 2), lesions with enhancement velocity beyond the malignancy threshold were found. 72% or 75% of lesions resolved completely during follow-ups. 69% of lesions were focal with irregular border. Time/signal intensity diagrams were almost always not suspicious; no wash-out phenomenon was seen. CONCLUSION: In MR mammography of premenopausal breast parenchyma, focal contrast enhancing lesions-even with enhancement beyond the malignancy threshold-may occur without any underlying pathology.
PURPOSE: The value of T2 weighted turbo-spin-echo sequences with selective fat suppression (TSE-SPIR) in the detection and differential diagnosis of focal liver lesions was compared to TSE sequences and conventional T1 weighted spin-echo (T1 SE) sequences at 0.5T. METHODS: In 50 patients with focal liver lesions T1 SE-TSE-, and TSE-SPIR sequences were performed. Two independent readers evaluated the sequences with regard to the image quality, fat suppression, and the number and conspicuity of liver lesions. Quantitative analysis was performed by tumour-liver contrast-to-noise (CNR) measurements. RESULTS: From a total of 118 liver lesions the T1 SE sequence, the TSE sequence, and the TSE-SPIR sequence showed 85.6%, 83.9%, and 91.5%, respectively (p < 0.05). The tumour-liver CNR of malignant liver lesions was 30.2-46.6% higher on the TSE-SPIR sequence compared to the TSE sequence (p < 0.01). With the exception of fat-containing lesions there was no significant difference of CNR in benign lesions on both TSE sequences. CONCLUSION: With regard to lesion detection the TSE-SPIR sequence is superior to the TSE sequence without fat suppression, whereas it is inferior to the TSE sequence in the differential diagnosis of benign and malignant lesions.
PURPOSE: Aim of the study was to evaluate FLAIR combined with Turbo-Spin-Echo (Turbo-FLAIR) at 0.5 tesla in comparison to conventional T1- and T2-weighted spin-echo images (SE) in MRI of the brain. MATERIAL AND METHODS: A Turbo-FLAIR sequence was optimised for 0.5 Tesla (Philips Gyroscan T5-II) that provided seventeen 5 mm sections in 4:21 minutes (TR = 6075 ms, T1 = 1600 ms, TE = 120 ms and a turbofactor = 17). Images were compared with T1- (TR = 500 ms, TE = 15 ms) proton density and T2-weighted spin-echo (TR = 2500 ms, TE = 20/90 ms) studies in 10 healthy volunteers and 30 patients with various brain pathologies. RESULTS: Turbo-FLAIR could effectively eliminate the CSF signal in all studies except ventricular areas with CSF inflow. Contrast-to-noise ratios (C/N) for the contrast between lesions and CSF was superior in Turbo-FLAIR. C/N between lesions and grey matter was significantly higher in Turbo-FLAIR than in proton density (PD)-weighted SE. C/N between lesions and white matter was equal to PD-weighted SE but significantly smaller than on T2-weighted SE. Visual analysis showed greater lesions conspicuity with Turbo-FLAIR and a higher frequency of detection of cortical and subcortical lesions. CONCLUSIONS: Turbo-FLAIR is a reliable and practical technique on 0.5 Tesla, that is more sensitive than SE sequences especially for the detection of cortical, subcortical lesions and lesions surrounded by CSF.
Protein translocation into the mammalian endoplasmic reticulum requires the Sec61p complex, which consists of three membrane proteins. The alpha-subunit, the homologue of Sec61p of yeast, shows some similarity to SecYp, a key component of the protein export apparatus of bacteria. In Escherichia coli, SecYp is also associated with two other proteins (SecEp and band-1 protein). We have now determined the sequences of the beta- and gamma-subunits of the mammalian Sec61p complex. Sec61-gamma is homologous to SSS1p, a suppressor of sec61 mutants in Saccharomyces cerevisiae, and can functionally replace it in yeast cells. Moreover, Sec61-gamma and SSS1p are structurally related to SecEp of E. coli and to putative homologues in various other bacteria. At least two subunits of the Sec61/SecYp complex therefore seem to be key components of the protein translocation apparatus in all classes of organisms.
In teamwork with agricultural schools data were collected by questionnaire, concerning management and housing of calves. Aim of the study is to get an overview about actual husbandry systems, and to allow some evaluation of application of ethological knowledge in practice. The results concerning different dimensions of system-details are interpreted widely being full-filled in terms of animal welfare legislation (Switzerland). Concerning more qualitative requirements it is found that application of animal welfare knowledge should be increased.
Ubiquitin-conjugating enzymes function in selective proteolysis pathways and catalyse the covalent attachment of ubiquitin to proteolytic substrates. Here we report the identification of an integral membrane ubiquitin-conjugating enzyme. This enzyme, UBC6, localizes to the endoplasmic reticulum (ER), with the catalytic domain facing the cytosol. ubc6 loss-of-function mutants suppress the protein translocation defect caused by a mutation in SEC61, which encodes a key component of a multisubunit protein translocation apparatus of the ER. The expression of the sec61 mutant phenotype requires both the activity of UBC6 and its localization at the ER membrane. This suggests that UBC6 may mediate selective degradation of ER membrane proteins and that the protein translocation defect of sec61 may be caused by proteolysis of components of a structurally distorted mutant translocation apparatus.
Attachment of ubiquitin to proteins is catalyzed by a family of ubiquitin-conjugating (UBC) enzymes. Although these enzymes are essential for many cellular processes; their molecular functions remain unclear because no physiological target has been identified for any of them. Here we show that four UBC proteins (UBC4, UBC5, UBC6, and UBC7) target the yeast MAT alpha 2 transcriptional regulator for intracellular degradation by two distinct ubiquitination pathways. UBC6 and UBC7 define one of the pathways and can physically associate. The UBC6/UBC7-containing complex targets the Deg1 degradation signal of alpha 2, a conclusion underscored by the finding that UBC6 is encoded by DOA2, a gene previously implicated in Deg1-mediated degradation. These data reveal an unexpected overlap in substrate specificity among diverse UBC enzymes and suggest a combinatorial mechanism of substrate selection in which UBC enzymes partition into multiple ubiquitination complexes.
Selective degradation of cellular proteins serves to eliminate abnormal proteins and to mediate the turnover of certain short-lived proteins, many of which have regulatory functions. In eukaryotes a major pathway for selective protein degradation is ATP-dependent and is mediated by the ubiquitin system. This pathway involves substrate recognition by components of a ubiquitin-protein ligase system, covalent attachment of ubiquitin moieties to proteolytic substrates, and subsequent degradation of these conjugates by a multicatalytic protease complex. Recent genetic evidence suggests that the remarkable selectivity of this process is largely controlled at the level of substrate recognition by the ubiquitin ligase system. In Saccharomyces cerevisiae, ubiquitin-conjugating enzymes UBC1, UBC4 and UBC5 have been identified as key components of this highly conserved degradation pathway. Genetic analysis indicates that ubiquitin-dependent proteolysis is essential for cell viability and that UBC4 and UBC5 enzymes are essential components of the eukaryotic stress response.
Covalent attachment of ubiquitin to cellular proteins is essential for cell viability and is catalysed by a set of distinct ubiquitin-conjugating enzymes. Individual members of this novel enzyme family mediate strikingly diverse functions, including DNA repair, cell cycle control, selective protein degradation and essential functions of the stress response.
Several physiological reactions including the sexual differentiation of the ascomycete Neurospora crassa are triggered by blue light. Mutants in the white-collar genes wc-1 and wc-2 are blind for all the blue light effects tested so far. We have previously shown that blue light induces some translatable mRNAs at different times after beginning the illumination. Here we report the cDNA cloning of four genes that are induced by blue light. Induction of these transcripts is temporally ordered (lag times from 2 to 45 min). Analysis of run-on transcripts show that the increases in mRNA levels are due to de novo transcription. None of these transcripts is inducible in white-collar mutants.
The effects of carvedilol, a new vasodilating beta-blocking drug, were studied in experimental pigs during short-term acute myocardial ischemia. In 21 anesthetized pigs 0.01, 0.03, and 0.1 mg/kg b.w. carvedilol was studied during repeated 2-min distal LAD-occlusions and a 60-min-period of ischemia. Left ventricular volume was continuously measured by the impedance catheter method. Intravenous administration of 0.01 mg/kg carvedilol resulted in a significant decrease of heart rate (-13%), dp/dtmax (-32%), and ejection fraction (-9%), slight changes of systolic pressure (-3%), and an increase of vascular resistance (+24%), indicating a beta-blocker effect without vasodilation-while the first vasodilatory effect was found at a dose of 0.1 mg/kg. During ischemia carvedilol had no influence on the time-course or the extent of systolic bulging of the ischemic myocardium, but the ischemia-induced decrease of left ventricular ejection fraction was diminished. Both during short-term ischemia, as well as during the 60-min-ischemia-period carvedilol significantly reduced ventricular premature beats. During the 60-min-ischemia-period activation delay measured from local DC-electrograms of the ischemic myocardium, as well as the occurrence of activation block were not altered by carvedilol, as was the incidence of ventricular fibrillation (69%). We conclude that at low dosages the beta-blocking effect of carvedilol exceeds the vasodilating properties. This may also hold true in patients with cardiac failure; they are more sensitive to beta-blocking drugs. During ischemia carvedilol slightly reduces the ischemia-dependent decrease of global ventricular function and it has an antiarrhythmic effect. Therefore, it may be protective in patients with acute myocardial infarction.
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We are reporting about an inoperable cell carcinoma of the stomach, which exclusively caused thoracal pains due to metastases into a pleural thickening. First this symptomatology with thoracal pains and recurring pleural effusions was thought to be a pleural mesothelioma. Only the immediate histological examination of the tissue showed the origin of the tumor. Although cancer of stomach appears very commonly, this tumor is often diagnosed too late and in most cases it is already inoperable. Even nowadays more than 75% of the patients with a cancer of the stomach die of their metastases, although diagnosis and therapy have been developed. - Pleural mesotheliomas are rare; nevertheless the possibility of a mesothelioma in connection with all pleural effusions of a vague genesis should be considered. The exposure to asbestos strengthens the suspicion that this tumor is existing. In connection with a pleural mesothelioma an indurative pleurisy, a primary cancer of the lung and - like in our case - pleural metastases of a primary cancer of another site have to be differentiated.
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A case of fibromuscular dysplasia (FMD) with involvement of the aorta is described in a 44-year-old woman. So far only 3 cases of aortal FMD have been mentioned, all in female patients. Our observation is characterized by a solitary stenosis of the lower abdominal aorta and it resembles histologically the "intimal fibroplasia" type of renal FMD. The review of the literature about FMD in general reveals that mostly the renal arteries are affected, followed by cervical artery FMD with only rare occurrence in other vessels. Though the etiology is basically unknown several factors have been made responsible, namely hereditary disposition, congenital rubella infection, female hormones, paucity of the vasa vasorum, and stretch-traction-stress. The disease has been classified into several histological subgroups and also according to the roentgenologic form which typically shows a "string of beads" appearance. There is a definitive female sex preponderance of 5:1, which is the same for all affected vessels; whereas in respect to age there is a marked distinction in so far that renal FMD patients on average are 11 years younger than patients with the cervicocephalic form of the disease.
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