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University of Düsseldorf

EducationDüsseldorf, Germany
About: University of Düsseldorf is a education organization based out in Düsseldorf, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 25225 authors who have published 49155 publications receiving 1946434 citations.


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Journal ArticleDOI
TL;DR: It is shown that selective nociceptive stimuli induce gamma oscillations in primary somatosensory cortex that are particularly related to the subjective perception of pain, and this findings support the hypothesis that Gamma oscillations arerelated to the internal representation of behaviorally relevant stimuli that should receive preferred processing.
Abstract: Successful behavior requires selection and preferred processing of relevant sensory information. The cortical representation of relevant sensory information has been related to neuronal oscillations in the gamma frequency band. Pain is of invariably high behavioral relevance and, thus, nociceptive stimuli receive preferred processing. Here, by using magnetoencephalography, we show that selective nociceptive stimuli induce gamma oscillations between 60 and 95 Hz in primary somatosensory cortex. Amplitudes of pain-induced gamma oscillations vary with objective stimulus intensity and subjective pain intensity. However, around pain threshold, perceived stimuli yielded stronger gamma oscillations than unperceived stimuli of equal stimulus intensity. These results show that pain induces gamma oscillations in primary somatosensory cortex that are particularly related to the subjective perception of pain. Our findings support the hypothesis that gamma oscillations are related to the internal representation of behaviorally relevant stimuli that should receive preferred processing.

347 citations

Journal ArticleDOI
TL;DR: It is concluded that oxygen plays a key role in the decomposition of sydnonimines and thus in the formation of NO as their pharmacodynamically active principle.
Abstract: The vasodilator and antiaggregatory properties of sydnonimines like SIN-1 are thought to be due to their marked stimulatory action on soluble guanylate cyclase. Enzyme activation and consecutive cyclic GMP accumulation is mediated by the liberation of nitric oxide (NO) from the open-ring A forms of sydnonimines. The purpose of the present study was to investigate the mechanism of NO release from sydnonimines in direct comparison to their stimulatory effect at the target enzyme, soluble guanylate cyclase. All sydnonimines tested were found to spontaneously liberate NO, the rate of which closely correlated with the extent of enzyme activation. NO release occurred nonlinearly with time and became maximal at high sydnonimine concentration. The in vitro stability of the A forms neither correlated with the measured rate of NO release nor with enzyme activation, indicating that a direct stimulation of guanylate cyclase by the A forms is rather unlikely. Besides NO, all sydnonimines generated NO2- and NO3- at a nearly equimolar rate. The addition of cysteine induced a marked shift from NO3- to NO2- with a small reduction in NO release, which is paralleled by a weak rightward shift of the EC50 at the guanylate cyclase. All tested sydnonimines were found to consume molecular oxygen at rates that closely corresponded to the measured rates of NO formation. By a molar comparison, the amounts of consumed oxygen are clearly higher, as would be expected for the oxidative conversion of NO to NO2- and NO3-. Oxygen seems to be additionally involved in the induction of NO formation while being converted to superoxide (O2-). In accordance with an autocatalytic process, O2- further enhances sydnonimine decomposition, since in the presence of superoxide dismutase (SOD) the rate of SIN-1C and NO2-/NO3- formation from SIN-1A was reduced, whereas the rate of NO liberation seemingly increased. O2- has, however, no influence on the rate of hydrolysis of SIN-1 to SIN-1A. At the level of guanylate cyclase, the presence of SOD induced a leftward shift of the concentration-response curve to SIN-1, in agreement with an enhancement of efficacy of NO by blocking the NO-scavenging effect of O2-. An additional O2- generation markedly enhanced SIN-1A decomposition to NO2-/NO3- and reduced the apparent rate of NO formation. We conclude from our results that oxygen plays a key role in the decomposition of sydnonimines and thus in the formation of NO as their pharmacodynamically active principle. Oxygen attack most probably occurs by one-electron abstraction from the A form of the respective sydnonimine compound.(ABSTRACT TRUNCATED AT 400 WORDS)

347 citations

Journal ArticleDOI
TL;DR: Primary analyses demonstrated that behaviour-changing interventions compared to no treatment/usual care control at longest follow-up reduced BMI, BMI z score and weight.
Abstract: Background: Child and adolescent overweight and obesity has increased globally, and can be associated with significant short- and longterm health consequences This is an update of a Cochrane Review published first in 2003, and updated previously in 2009 However, the update has now been split into six reviews addressing different childhood obesity treatments at different ages Objectives: To assess the effects of diet, physical activity and behavioural interventions (behaviour-changing interventions) for the treatment of overweight or obese children aged 6 to 11 years Search methods: We searched CENTRAL, MEDLINE, Embase, PsycINFO, CINAHL, LILACS as well as trial registers ClinicalTrialsgov and RsdI1401 Diet, physical activity and behavioural interventions for the treatment of overweight or obese children from th 2 / 499 ICTRP Search Portal We checked references of studies and systematic reviews We did not apply any language restrictions The date of the last search was July 2016 for all databases Selection criteria: We selected randomised controlled trials (RCTs) of diet, physical activity, and behavioural interventions (behaviour-changing interventions) for treating overweight or obese children aged 6 to 11 years, with a minimum of six months' follow-up We excluded interventions that specifically dealt with the treatment of eating disorders or type 2 diabetes, or included participants with a secondary or syndromic cause of obesity Data collection and analysis Two review authors independently screened references, extracted data, assessed risk of bias, and evaluated the quality of the evidence using the GRADE instrument We contacted study authors for additional information We carried out metaanalyses according to the statistical guidelines in the Cochrane Handbook for Systematic Reviews of Interventions Main results: We included 70 RCTs with a total of 8461 participants randomised to either the intervention or control groups The number of participants per trial ranged from 16 to 686 Fifty-five trials compared a behaviour-changing intervention with no treatment/usual care control and 15 evaluated the effectiveness of adding an additional component to a behaviour-changing intervention Sixty-four trials were parallel RCTs, and four were cluster RCTs Sixty-four trials were multicomponent, two were diet only and four were physical activity only interventions Ten trials had more than two arms The overall quality of the evidence was low or very low and 62 trials had a high risk of bias for at least one criterion Total duration of trials ranged from six months to three years The median age of participants was 10 years old and the median BMI z score was 22 Primary analyses demonstrated that behaviour-changing interventions compared to no treatment/usual care control at longest follow-up reduced BMI, BMI z score and weight Mean difference (MD) in BMI was -053 kg/m2 (95% confidence interval (CI) -082 to -024); P < 000001; 24 trials; 2785 participants; low-quality evidence MD in BMI z score was -006 units (95% CI -010 to -002); P = 0001; 37 trials; 4019 participants; low-quality evidence and MD in weight was -145 kg (95% CI -188 to -102); P < 000001; 17 trials; 1774 participants; low-quality evidence Thirty-one trials reported on serious adverse events, with 29 trials reporting zero occurrences RR 057 (95% CI 017 to 193); P = 037; 4/2105 participants in the behaviour-changing intervention groups compared with 7/1991 participants in the comparator groups) Few trials reported health-related quality of life or behaviour change outcomes, and none of the analyses demonstrated a substantial difference in these outcomes between intervention and control In two trials reporting on minutes per day of TV viewing, a small reduction of 66 minutes per day (95% CI -1288 to -031), P = 004; 2 trials; 55 participants) was found in favour of the intervention No trials reported on all-cause mortality, morbidity or socioeconomic effects, and few trials reported on participant views; none of which could be meta-analysed As the meta-analyses revealed substantial heterogeneity, we conducted subgroup analyses to examine the impact of type of comparator, type of intervention, risk of attrition bias, setting, duration of post-intervention follow-up period, parental involvement and baseline BMI z score No subgroup effects were shown for any of the subgroups on any of the outcomes Some data indicated that a reduction in BMI immediately post-intervention was no longer evident at follow-up at less than six months, which has to be investigated in further trials Authors' conclusions: Multi-component behaviour-changing interventions that incorporate diet, physical activity and behaviour change may be beneficial in achieving small, short-term reductions in BMI, BMI z score and weight in children aged 6 to 11 years The evidence suggests a very low occurrence of adverse events The quality of the evidence was low or very low The heterogeneity observed across all outcomes was not explained by subgrouping Further research is required of behaviourchanging interventions in lower income countries and in children from different ethnic groups; also on the impact of behaviour-changing interventions on health-related quality of life and comorbidities The sustainability of reduction in BMI/BMI z score and weight is a key consideration and there is a need for longer-term follow-up and further research on the most appropriate forms of post-intervention maintenance in order to ensure intervention benefits are sustained over the longer term

347 citations

Journal ArticleDOI
TL;DR: The consistent association of a poor psychosocial quality of work with intended early retirement among older employees across all European countries under study calls for improved investments into betterquality of work, in particular increased control and an appropriate balance between efforts spent and rewards received at work.
Abstract: Background: Given the challenge of a high proportion of older employees who retire early from work we analyse associations of indicators of a poor psychosocial quality of work with intended premature departure from work in a large sample of older male and female employees in 10 European countries. Methods: Baseline data from the 'Survey of Health, Ageing and Retirement in Europe' (SHARE) were obtained from 3523 men and 3318 women in 10 European countries. Data on intended early retirement, four measures of well-being (self-rated health, depressive symptoms, general symptom load, and quality of life), and quality of work (effort-reward imbalance; low control at work) were obtained from struc- tured interviews and questionnaires. Country-specific and total samples are analysed, using logistic regression analysis. Results: Poor quality of work is significantly associated with intended early retire- ment. After adjustment for well-being odds ratios (OR) of effort-reward imbalance (OR 1.72 (1.43-2.08)) and low control at work (OR 1.51 (1.27-1.80)) on intended early retirement are observed. Poor quality of work and reduced well-being are independently associated with the intention to retire from work. Conclusion: The consistent association of a poor psychosocial quality of work with intended early retire- ment among older employees across all European countries under study calls for improved investments into better quality of work, in particular increased control and an appropriate balance between efforts spent and rewards received at work.

346 citations

Journal ArticleDOI
TL;DR: It was found that thiosulfate was excreted in massive amounts in urine of both Ethe1−/− mice and humans with ethylmalonic encephalopathy, and ETHE1 is a mitochondrial sulfur dioxygenase involved in catabolism of sulfide that accumulates to toxic levels in ethyl malonicEncephalopathy.
Abstract: Ethylmalonic encephalopathy is an autosomal recessive developmental disorder that is characterized by chronic diarrhea and multiple neurological deficits. It is associated with loss-of-function mutations in the ETHE1 gene. Now, Massimo Zeviani and his colleagues report that ETHE1 is a dioxygenase that is responsible for breaking down toxic sulfide in a variety of organs. Ethylmalonic encephalopathy is an autosomal recessive, invariably fatal disorder characterized by early-onset encephalopathy, microangiopathy, chronic diarrhea, defective cytochrome c oxidase (COX) in muscle and brain, high concentrations of C4 and C5 acylcarnitines in blood and high excretion of ethylmalonic acid in urine. ETHE1, a gene encoding a β-lactamase–like, iron-coordinating metalloprotein, is mutated in ethylmalonic encephalopathy. In bacteria, ETHE1-like sequences are in the same operon of, or fused with, orthologs of TST, the gene encoding rhodanese, a sulfurtransferase. In eukaryotes, both ETHE1 and rhodanese are located within the mitochondrial matrix. We created a Ethe1−/− mouse that showed the cardinal features of ethylmalonic encephalopathy. We found that thiosulfate was excreted in massive amounts in urine of both Ethe1−/− mice and humans with ethylmalonic encephalopathy. High thiosulfate and sulfide concentrations were present in Ethe1−/− mouse tissues. Sulfide is a powerful inhibitor of COX and short-chain fatty acid oxidation, with vasoactive and vasotoxic effects that explain the microangiopathy in ethylmalonic encephalopathy patients. Sulfide is detoxified by a mitochondrial pathway that includes a sulfur dioxygenase. Sulfur dioxygenase activity was absent in Ethe1−/− mice, whereas it was markedly increased by ETHE1 overexpression in HeLa cells and Escherichia coli. Therefore, ETHE1 is a mitochondrial sulfur dioxygenase involved in catabolism of sulfide that accumulates to toxic levels in ethylmalonic encephalopathy.

346 citations


Authors

Showing all 25575 results

NameH-indexPapersCitations
Karl J. Friston2171267217169
Roderick T. Bronson169679107702
Stanley B. Prusiner16874597528
Ralph A. DeFronzo160759132993
Monique M.B. Breteler15954693762
Thomas Meitinger155716108491
Karl Zilles13869272733
Ruben C. Gur13674161312
Alexis Brice13587083466
Michael Schmitt1342007114667
Michael Weller134110591874
Helmut Sies13367078319
Peter T. Fox13162283369
Yuri S. Kivshar126184579415
Markus M. Nöthen12594383156
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023139
2022470
20213,130
20202,720
20192,507
20182,439